C-19 Archives

A raven’s overview

Sun, 25 Jan 2026 18:00:26 GMT

‘Prevention wasn’t impossible. It was withheld...

In people with pre-existing dementia, SARS-CoV-2 infection is repeatedly associated with faster cognitive decline.

For families, that can mean the difference between years at home and a rapid fall over months.’

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❦ On fatal silence

By Zdeněk Vrožina MBA (25 Jan 2026)

❦ ‘1. COVID-19 infection during pregnancy is not a neutral event.

Inflammation, viral proteins, and especially COVID-specific impairment of placental blood-flow can affect fetal development – and abnormalities in exposed newborns are being reported with increasing consistency across studies.

That infection during pregnancy increases the risk of neurodevelopmental difficulties – in speech, motor skills, attention, and learning – has been known in public-health and medical circles for years.

Mothers were simply not told.

This wasn’t ignorance. It was a decision to downplay the risk.

‘ That infection during pregnancy increases the risk of neurodevelopmental difficulties – in speech, motor skills, attention, and learning – has been known in public-health and medical circles for years. ’

❦ 2. Are you constantly sick since COVID? Are your children?

Public health may have avoided telling you an uncomfortable truth – for many people, after SARS-CoV-2 infection, the immune system does not work the same way as before.

Changes in immune-cell numbers, functional exhaustion, and impaired co-ordination between innate and adaptive immunity mean one thing – infections that used to pass in the background now last longer, recur, or come in chains.

Recovery of immune function is uncertain.

‘ Changes in immune-cell numbers, functional exhaustion, and impaired co-ordination between innate and adaptive immunity mean one thing – infections that used to pass in the background now last longer, recur, or come in chains. ’

❦ 3. “Kids will be fine.”

It sounded reassuring. But public health knew that infection-induced neuroinflammation and vascular changes can affect cognition – in children as well as adults.

They didn’t tell you.

And now the consequences are already visible in schools – worse attention, slower information processing, higher cognitive fatigue, and measurable declines in standardized cognitive scores, including IQ.

If prevention of repeated infections in schools is ignored, children will carry the burden.

Not moral consequences. Biological ones.

‘ And now the consequences are already visible in schools – worse attention, slower information processing, higher cognitive fatigue, and measurable declines in standardized cognitive scores, including IQ. ’

❦ 4. Depression. A trendy explanation for the surge in mental-health problems among children.

But the data don’t fully support that story.

Multiple follow-up studies show that the risk of depression, anxiety, and mood disorders is significantly and consistently higher in children who had SARS-CoV-2 infection.

This is not a uniform pandemic stress effect. It’s not mainly lockdowns, smartphones, or social media.

Infection itself is an independent biological risk factor.

And the neuro-immune mechanisms – neuroinflammation, altered serotonin and dopamine pathways, HPA-axis disruption – have been described in the literature for years.

They just weren’t communicated to the public.

‘ Multiple follow-up studies show that the risk of depression, anxiety, and mood disorders is significantly and consistently higher in children who had SARS-CoV-2 infection.

And the neuro-immune mechanisms – neuroinflammation, altered serotonin and dopamine pathways, HPA-axis disruption – have been described in the literature for years. ’

❦ 5. After every major COVID wave, the same pattern appears – first the respiratory phase… then cardiovascular aftershocks – clots, heart attacks, strokes.

At the individual level, it’s even clearer.

After a mild COVID infection, there is a higher relative risk of cardiovascular complications – ischemic heart disease, arrhythmias, thrombosis, stroke.

The most frustrating part?

These are often working-age adults. One infection increases the probability of an event that can change the rest of your life.

‘ After every major COVID wave, the same pattern appears – first the respiratory phase… then cardiovascular aftershocks – clots, heart attacks, strokes. ’

And prevention was simple.

If public health had openly said that risk exists even after mild COVID, some people might have avoided life-long consequences.

Instead, the system failed the very people who fund it.

‘ At the individual level, it’s even clearer. After a mild COVID infection, there is a higher relative risk of cardiovascular complications – ischemic heart disease, arrhythmias, thrombosis, stroke. ’

❦ 6. And don’t assume cardiovascular effects spare children. They don’t.

A growing number of studies show that even previously healthy children can have subclinical cardiac changes after SARS-CoV-2 infection.

Invisible. Not routinely screened. But biologically real. A ten-year-old not having a heart attack does not mean nothing happened.

❦ 7. For people who don’t yet have cancer, a single SARS-CoV-2 infection can disrupt anti-tumor immune surveillance, beyond the acute phase.

For patients who already have cancer, COVID is well documented to complicate oncologic care and worsen outcomes – through biological stress, immune disruption, reduced tolerance.

This is not new information.

What’s new is that patients were rarely told that reducing infection risk is part of protecting prognosis.

Prevention wasn’t impossible. It was withheld.

‘ For patients who already have cancer, COVID is well documented to complicate oncologic care and worsen outcomes – through biological stress, immune disruption, reduced tolerance. ’

❦ 8. What about your parents? Did you notice a sudden decline in memory, orientation, speech, or attention after COVID?

In people with pre-existing dementia, SARS-CoV-2 infection is repeatedly associated with faster cognitive decline.

For families, that can mean the difference between years at home and a rapid fall over months.

‘ In people with pre-existing dementia, SARS-CoV-2 infection is repeatedly associated with faster cognitive decline.

For families, that can mean the difference between years at home and a rapid fall over months. ’

At the population level, studies also show an increased risk of new dementia diagnoses after infection. For older adults, a single infection can accelerate the trajectory of decline.

Silence from public health fills nursing homes and clinics faster than anything else.

❦ 9. Repeated infections?

Herd exposure as immune training stopped making sense once immune dysregulation became clear. After SARS-CoV-2 infection, parts of the immune system may no longer function normally.

Weakened interferon responses, impaired antigen presentation via MHC-I, exhausted T cells, disrupted immune surveillance.

Public health has known this for years. They didn’t tell you.

And that’s why each additional infection is no longer neutral – it’s another hit to a system that has already lost balance.

‘ Herd exposure as immune training stopped making sense once immune dysregulation became clear.

Weakened interferon responses, impaired antigen presentation via MHC-I, exhausted T cells, disrupted immune surveillance.

Public health has known this for years. ’

❦ 10. This essay is about information that already existed. Public health had it. The public did not.

Without information, there is no informed choice. Only consequences.

This wasn’t about people refusing to protect themselves. They were never told why it mattered. When you hide risk, you don’t take away freedom. You take away the chance to choose.

‘ Without information, there is no informed choice. Only consequences. ’

The greatest failure of the pandemic was not the virus. It was the silence.

The consequences are not a few weeks of fatigue. A significant share of people are now living in a chronic, often progressive condition.

The estimated price tag of $3.7 trillion in the United States. Approximately 1 trillion CZK in the Czech Republic.

Public health silence has translated into a permanent loss of functional capacity across society – lower labor-force participation, reduced productivity, and measurable drag on GDP.

Never in modern history has such a small number of decision-makers, through flawed public-health choices, caused damage on this scale.’

‘ Public health silence has translated into a permanent loss of functional capacity across society – lower labor-force participation, reduced productivity, and measurable drag on GDP.

Never in modern history has such a small number of decision-makers, through flawed public-health choices, caused damage on this scale. ’

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By Zdeněk Vrožina MBA (25 Jan 2026) ➤

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More on... Public Health

More... Essays and Comment

✾ On SARS-CoV-2 (COVID-19), brain damage, neurological damage, and dementia

Fri, 21 Nov 2025 21:08:39 GMT

‘Although COVID-19 was originally considered a respiratory illness, it is now well established that SARS-CoV-2 infection can have far-reaching impacts on the nervous system.

Common neurological symptoms in Long COVID [PASC] include new-onset cognitive difficulties, dysautonomia, fatigue, and peripheral neuropathy.’

from ‘Neuroimmune pathophysiology of long COVID’ by Moen et al / Psychiatry and Clinical Neurosciences (2025).

❦ Dysautonomia is a condition in which the autonomic nervous system ( ANS ) does not work properly. This condition may affect the functioning of the heart , bladder , intestines , sweat glands , pupils , and blood vessels .

❦ A 42-minute read.

�� (5 Jul 2023 ~ The Lancet Regional Health: Western Pacific) Post-COVID cognitive dysfunction: current status and research recommendations for high risk population ➤

‘ Post-COVID cognitive dysfunction ( PCCD ) is a condition in which patients with a history of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection, usually three months from the onset, exhibit subsequent cognitive impairment in various cognitive domains , and cannot be explained by an alternative diagnosis.

The clinical manifestations of COVID-19 [ SARS-2 ] range from asymptomatic to fatal.

Post-COVID-19 conditions are characterized by multi-organ structural and functional impairment , including cardiovascular , neurological , psychiatric , hematological , pulmonary , and dermatological injury.

Although COVID-19 primarily presents as a respiratory infection with flu-like symptoms , it is now considered a multi-organ disease , often involving the nervous system .

Recent evidence indicates that approximately 80% of people who are infected with COVID-19 have one or more long-term symptoms . ’

�� (23 Jan 2025 ~ PLOS Medicine) Persistent symptoms and clinical findings in adults with Post-Acute Sequelae of COVID-19 / Post-COVID-19 Syndrome (PCS) in the second year after acute infection ➲

‘ Many patients with persistent Post-COVID-19 Syndrome [ PASC ] show impaired executive functioning, reduced cognitive processing speed, and reduced physical exercise capacity. ’

�� (13 Sep 2022 ~ Science Daily / Journal of Alzheimer’s Disease) Risk for Developing Alzheimer’s Disease Increases by 50-80% In Older Adults Who Caught COVID-19 ➲

‘ Older people who were infected with COVID-19 show a substantially higher risk – as much as 50% to 80% higher than a control group – of developing Alzheimer’s disease within a year , according to a study of more than 6 million patients 65 and older .

And the highest risk was observed in women at least 85 years old .

The findings showed that the risk for developing Alzheimer’s disease in older people nearly doubled (0.35% to 0.68%) over a one-year period following infection with COVID-19 . ’

�� (19 Apr 2023 ~ Nature Scientific Reports) Cognitive impairment in young adults with post COVID-19 syndrome ➤

‘ Regarding the different cognitive functions, our results reveal that attention is the one that shows the greatest deficit, regardless of the age of the patients ( more than 25% of patients in each age group exhibit a moderate attention deficit ).

Processing speed was also a cognitive process that was impaired relatively homogeneously across age groups; however, the results indicate that the youngest patients show a much slower processing speed ( 33.3% of those under 50 years of age) compared to the oldest ( 5.1% of those over 50 years of age).

The highest percentage of patients with severe verbal memory impairment was also found in the younger patients group.

In long-term memory , 20.7% of the youngest group showed a severe deficit and 24.1% a mild impairment , while a minimum proportion of the elderly showed alterations in this area.

The results presented here reveal that at least 85% of the participants exhibit deficits in one neuropsychological test.

Also, the youngest patients were those who showed the most marked and heterogeneous cognitive impairment . ’

�� (27 Feb 2024 ~ Nature Scientific Reports) Neuroimaging findings in children with COVID-19 infection: a systematic review and meta-analysis ➤

‘ Initially focused on respiratory symptoms, it’s now clear that COVID-19 presents a complex clinical picture affecting various organ systems.

Our findings reveal that a substantial proportion of pediatric COVID-19 patients with neurological symptoms exhibit abnormal neuroimaging findings, with 43.74% of children in the included studies demonstrating such abnormalities. ’

�� (11 Nov 2025 ~ Nature Pediatric Research) Neurological and neurodevelopmental effects of Covid and MIS-C on children ➤

‘ While the respiratory symptoms of COVID-19 have dominated the early narratives of the disease, it has become increasingly clear that the virus’s impact stretches far beyond the lungs.

The pediatric population, once thought to be relatively spared from severe outcomes, has presented with significant neurological manifestations that raise concerns about the short- and long-term effects of SARS-CoV-2 on the developing nervous system. ’

Lay-person’s overview: �� (12 Nov 2025 ~ Bioengineer) Neurological Impacts of COVID and MIS-C in Children ➤

�� (16 Jan 2023 ~ Brain) Haemorrhage of human foetal cortex associated with SARS-CoV-2 infection ➤

‘ Strikingly, the [ foetal brain ] haemorrhages are predominantly found in the late first and early second trimester of gestation.

Specifically, the majority were between 12 and 14 PCW [ post-conception week ] , a critical window of human foetal brain development when the endothelial tight junctions increase to form the blood-brain barrier (BBB).

Our observations of disrupted foetal cerebral vasculature are consistent with reports of damage to the microvasculature of the adult brain in SARS-CoV-2 infected patients. ’

�� (1 Oct 2023 ~ New Atlas / Nature Communications) All variants of COVID-19 can infect the brain, study finds ➲

‘ Interestingly, the findings confirmed epidemiological observations showing acute disease severity is reduced in Omicron infections – however, all [ SARS-CoV-2 ] variants demonstrated similar neuroinvasive capabilities .

And, most strikingly, all variants infected the brain’s olfactory regions regardless of whether symptoms of anosmia (the loss of sense of smell) were present or not. ’

�� (30 Aug 2023 ~ Trends in Cognitive Sciences) Effects of COVID-19 on cognition and brain health ➤

‘ Executive dysfunction is a commonly reported effect in the acute stage , especially in patients over 60 years of age with moderate to severe acute symptoms. ’

‘Researchers have found evidence that the COVID-causing virus, SARS-CoV-2 , can reach the brain and other parts of the central nervous system . This contact may lead to persistent and devastating symptoms of PASC ( Post-Acute Sequelae of COVID-19 , or ‘long COVID’), which – more and more scientists say – appears to be a neurological disease .

Cognitive symptoms include difficulty thinking and remembering things .

And physical ailments , such as pain , extreme fatigue and a racing heartbeat , are tied to problems with the autonomic nervous system , which ordinarily runs our bodies on autopilot.’

From (1 Mar 2023 ~ Scientific American) Long COVID now looks like a neurological disease, helping doctors to focus treatments ➤

�� (19 Jun 2025 ~ Psychiatry and Clinical Neurosciences) Neuroimmune pathophysiology of long COVID ➤

‘ Despite the perception that COVID-19 is now a mild disease, there is overwhelming evidence indicating that SARS-CoV-2 infection is capable of producing widespread post-acute sequelae in a significant percentage of infections.

This includes a substantial impact on the nervous system resulting from a combination of direct infection, systemic inflammation, immune dysfunction, vascular complications, and tissue hypoxia. ’

❦ Brain damage is a term that describes the destruction or degeneration of brain cells , which can result from various causes such as trauma , stroke , tumours , infection , lack of oxygen , or other illnesses .

Brain damage can be categorised into two main types :

Traumatic Brain Injury ( TBI ), caused by an external force like a blow to the head or a penetrating object

and Acquired Brain Injury ( ABI ), which occurs at the cellular level and is often associated with conditions like stroke , tumours , or anoxia .

Significant ABI can be caused by viral , bacterial and fungal infections .

Brain damage can be focal – affecting a specific area – or diffuse , involving multiple areas of the brain.

Brain damage can lead to a range of impairments in cognitive , physical , emotional , or independent functioning – including problems with

memory
attention
reasoning
speech
motor-control (eg. balance)
and psychosocial behaviour .

�� (22 Feb 2024 ~ Nature Neuroscience) Blood-brain barrier disruption and sustained systemic inflammation in individuals with long COVID-associated cognitive impairment ➲

‘ Our data suggest that sustained systemic inflammation and persistent localized blood-brain barrier (BBB) dysfunction is a key feature of long COVID-associated brain fog.

Patients with long COVID had elevated levels of IL-8, GFAP and TGFβ – with TGFβ specifically increased in the cohort with brain fog.

GFAP is a robust marker of cerebrovascular damage and is elevated after repetitive head trauma , reflecting BBB disruption, as seen in contact sport athletes and in individuals with self-reported neurological symptoms in long COVID .

Interestingly, TGFβ was strongly associated with BBB disruption and structural brain changes. ’

�� (20 March 2025 ~ Interview with David Putrino ~ Radio-Canada / Canadian Broadcasting Corporation) Beyond Long COVID – How reinfections could be causing silent long-term organ damage ➤

“ There was a recent 2024 study showing us that individuals who survive an acute COVID-19 infection – these are not individuals who are getting diagnosed with long COVID – on average will lose somewhere in the neighbourhood of two to six IQ points per infection.

For the longest time in the field of immunology, there was the sort of adage that your immune system needs to be tested every now and again to stay strong.

That’s an old-fashioned idea.

The more new-fashioned and evidence-based idea is that, although your immune system can take on an infection, you want to avoid testing it as much as possible because your body is sustaining damage with each infection that it survives . ”

❦ SARS-CoV-2 (COVID-19) infections can lead to short- or long-term health effects in nearly every organ system of the body.

✺ Nervous System

Stroke
Headaches
Memory problems
Problems with smell & taste.

✺ Mental Health

Anxiety
Depression
Sleep problems
Substance abuse.

✺ Gastrointestinal System

Constipation
Diarrhoea
Acid reflux.

✺ Skin Disorders

Rash
Hair loss.

✺ Coagulation Disorders

Blood clots.

✺ Respiratory System

Cough
Shortness of breath
Low blood oxygen.

✺ Cardiovascular System

Acute coronary disease
Heart failure
Palpitations
Arrythmias.

✺ Musculoskeletal System

Joint pain
Muscle weakness.

✺ Metabolic / Endocrine System

Obesity
Diabetes
High cholestrol.

✺ Kidney

Acute kidney injury
Chronic kidney disease (CKD).

✺ General

Fatigue
Malaise
Anaemia.

�� (16 Jan 2024 ~ American Heart Association) Beyond breathing: How COVID-19 affects your heart, brain and other organs ➲

“ I would argue that COVID-19 is not a disease of the lungs at all.

It seems most likely that it is what we call a vascular and neurologic infection, affecting both nerve endings and our cardiovascular system. ”

“In addition to the cognitive impairment, we see worsening or new-onset migraines. We see new neuropathy in the legs and the arms – numbness, tingling, difficulty walking – because of the neuropathy. ”

�� (22 Sep 2022 ~ Nature Medicine) Long-term neurologic outcomes of COVID-19 ➤

‘ Our results show that in the post-acute phase of COVID-19, there was increased risk of an array of incident neurologic sequelae including ischemic and hemorrhagic stroke, cognition and memory disorders, peripheral nervous system disorders, episodic disorders (for example, migraine and seizures), extrapyramidal and movement disorders, mental health disorders, musculoskeletal disorders, sensory disorders, Guillain-Barré syndrome, and encephalitis or encephalopathy. ’

‘ Arterial thrombosis is a notable occurrence in COVID-19 patients, leading to various complications, such as acute ischemic stroke ( AIS ), acute coronary syndrome ( ACS ), acute limb ischemia ( ALI ), mesenteric infarction , renal infarction , and spleen infarction .’

Image: �� 1 Aug 2025 ~ Frontiers in Immunology) COVID-19: a vascular nightmare unfolding ➤

❦ ‘The incidence of hospitalisation with cerebral infarction [ ischaemic stroke ] was twice as high after COVID‐19 onset.

Other investigators have estimated the risk of stroke to be 2–13 times as high for people with COVID‐19.’ (The Medical Journal of Australia ~ 2022) ➲

�� (15 Jul 2023 ~ Acta Neuropathologica) Vagus nerve inflammation contributes to dysautonomia in COVID-19 ➤

‘ Our data suggest that SARS-CoV-2 induces vagus nerve inflammation, followed by autonomic dysfunction, which contributes to critical disease courses.

The vagus nerve could be particularly susceptible to SARS-CoV-2 infection as it is directly innervating the respiratory tract, which is the primary site of infection. ’

❦ Inflammation of the vagus nerve can lead to autonomic dysfunction, or ‘dysautonomia’.

✺ Autonomic dysfunction ( dysautonomia ) is a group of disorders affecting the autonomic nervous system ( ANS ).

➲ Signs of autonomic dysfunction include:

Tachycardia (fast heart-rate)
Orthostatic hypotension (dizziness or fainting upon standing)
Gastrointestinal disorders (e.g. constipation, diarrhoea, loss of appetite, difficulty swallowing, difficulty digesting food)
Disturbed bladder function (e.g. incontinence, difficulty starting urination, incomplete emptying of the bladder)
Temperature dysregulation (e.g. sensitivity to heat or cold; cold, discoloured hands and feet)
Sexual dysfunction (e.g. difficulty with ejaculation or maintaining an erection; vaginal dryness)
Vision problems (e.g. inability of the pupils to react to light quickly; blurred vision)
Sleep problems .

�� (15 Jan 2025 ~ Molecular Psychiatry) Choroid plexus volume is enlarged in long COVID and associated with cognitive and brain changes ➤

‘ Patients with post-COVID condition (PCC/PASC) present with diverse symptoms which persist at long-term after SARS-CoV-2 infection.

Among these symptoms, cognitive impairment is one of the most prevalent and has been related to structural and functional changes in the brain.

Results revealed choroid plexus (ChP) volume enlargement in PCC patients compared to healthy controls.

The ChP enlargement was associated with cognitive dysfunction, grey matter volume reduction in frontal and subcortical areas, white matter integrity, diffusivity changes, and functional connectivity changes. ’

�� (7 Mar 2022 ~ Nature) SARS-CoV-2 is associated with changes in brain structure in UK Biobank ➤

‘ After infection with SARS-CoV-2, individuals show a greater reduction in grey matter thickness and tissue contrast in the orbitofrontal cortex and parahippocampal gyrus ; greater changes in markers of tissue damage in regions that are functionally connected to the primary olfactory cortex; and a greater reduction in global brain size.

Significantly greater cognitive decline was observed in the SARS-CoV-2-positive group, and this decline was associated with greater atrophy of crus II – a cognitive lobule of the cerebellum . ’

❦ Executive function

A set of cognitive processes that helps you manage tasks , make plans , solve problems , adapt to new situations , and control your emotions .

These skills involve working memory , cognitive flexibility , and inhibition control .

Damage to the brain’s prefrontal cortex and related areas can lead to executive dysfunction .

❦ Motor function

The ability of the body to perform movements through the co-ordination of the nervous system , muscles , and brain .

Motor function includes voluntary actions like walking , running or writing – and involuntary actions , such as reflexes .

Clumsiness and balance issues can be examples of motor dysfunction .

�� (10 Apr 2023 ~ Nature Scientific Reports) Cerebral hypoperfusion in post-COVID-19 cognitively impaired subjects revealed by arterial spin labeling MRI ➤

‘ The results showed a significant hypoperfusion in a widespread cerebral network in the post-COVID-19 group, predominantly affecting the frontal cortex, as well as the parietal and temporal cortex.

The hypoperfusion areas identified in the right hemisphere regions were more extensive.

These findings support the hypothesis of a large network dysfunction in post-COVID subjects with cognitive complaints. ’

�� (19 Jan 2024 ~ Nature Scientific Reports) Microstructural brain abnormalities, fatigue, and cognitive dysfunction after mild COVID-19 ➲

‘ We conducted a cross-sectional study of 97 consecutive subjects (median age of 41 years) after a mild infection, with a median of 79 days (and mean of 97 days) after diagnosis of COVID-19.

The patients reported memory loss (36%), fatigue (31%), and headache (29%).

The quantitative analyses confirmed symptoms of fatigue (83% of participants), excessive somnolence (35%), impaired phonemic verbal fluency (21%), impaired verbal categorical fluency (13%), and impaired logical memory immediate recall (16%).

Our results suggest persistent cognitive impairment and subtle white matter abnormalities in individuals mildly infected. ’

❦ Neuropsychological assessments

Verbal fluency tests are a standard component of neuropsychological assessment used to evaluate cognitive function and executive dysfunction , particularly in the context of brain damage , or neurodegenerative diseases like Alzheimer’s .

❦ Phonemic verbal fluency

A phonemic fluency test is a cognitive task where a participant is asked to generate as many words as possible beginning with a specific letter within a set time frame, typically one minute.

❦ Verbal categorical fluency

A categorical fluency test is a cognitive task where a participant is asked to produce as many words as possible from a category (for example animals, or fruits) in a given time (usually a minute).

❦ Logical memory immediate recall

A cognitive test designed to assess verbal episodic memory , where the examinee is read a narrative story and immediately asked to recall as many details from the story as possible.

�� (2 Feb 2025 ~ News Medical Life Sciences / Nature Medicine) Does COVID increase the risk of Alzheimer’s disease? ➤

‘ The study found that individuals who had COVID-19 exhibited significant changes in brain biomarkers associated with Alzheimer’s disease.

Strikingly, these biomarker changes were comparable to four years of aging.

Interestingly, even participants who had mild or asymptomatic COVID-19 showed alterations in their plasma biomarkers, suggesting that the infection’s impact on brain health may not be limited to severe cases.

The researchers also analyzed cognitive test scores and neuroimaging data, finding that COVID-19-positive individuals exhibited lower cognitive test performance compared to controls – equivalent to almost two years of age-related cognitive decline.

Brain imaging revealed structural patterns associated with Alzheimer’s disease in some participants, further reinforcing the potential link between COVID-19 and neurodegeneration. ’

�� (8 Jan 2024 ~ Frontiers in Aging Neuroscience) Unravelling the connection between COVID-19 and Alzheimer’s disease: a comprehensive review ➲

‘ [ SARS-CoV-2’s ] ability to invade the central nervous system through the hematogenous and neural routes, besides attacking the respiratory system, has the potential to worsen cognitive decline in Alzheimer’s disease patients.

SARS-CoV-2 infection causes immune system dysfunction, which can lead to suppression of neurogenesis, synaptic damage, and neuronal death, all of which are associated with the aetiology of Alzheimer’s disease.

COVID-19 causes a secondary effect on underlying brain pathologies, as SARS-CoV-2 has been shown to trigger or accelerate neurodegeneration processes that possibly explain long-term neurodegenerative effects in the elderly population. ’

❦ Dementia is a general term for a collection of symptoms that affect memory , thinking , language , problem-solving , and other cognitive abilities to a degree that interferes with daily life and activities.

It is not a single disease but rather an overall term to describe a range of neurological conditions affecting the brain that worsen over time .

These conditions include Alzheimer’s disease , which accounts for 50–70% of cases of dementia worldwide.

Other types of dementia include vascular dementia , dementia with Lewy bodies , frontotemporal dementia , and mixed dementia (commonly Alzheimer’s disease and vascular dementia).

Dementia is not a normal part of ageing , although it is more common in older people.

�� (3 Mar 2025 ~ Bloomberg UK) What We Know About Covid’s Impact on Your Brain ➲

‘ For patients already battling Alzheimer’s disease, studies indicate that Covid can exacerbate brain inflammation, damage immune cells, and accelerate the disease.

Even previously healthy older adults face an increased risk of cognitive impairment and new-onset dementia after infection. ’

�� (28 Jul 2021 ~ Neurodegenerative Diseases) The Impact of the COVID-19 Pandemic on Dementia Risk: Potential Pathways to Cognitive Decline ➲

‘ SARS-CoV-2 infection initiates a disease progression that has the potential to promote cognitive decline and exacerbate pre-existing dementia.

The damage cascade of COVID-19 is multi-faceted and interdependent, with multiple pathways that could lead to cognitive hazard mechanisms.

One such cognitive hazard mechanism, cerebral direct infection, is possible with the SARS-CoV-2 virus, exhibiting neuroinvasive and neurotropic characteristics with neurovirulent potential.

The greatest cognitive risk though may be from immune-mediated damage originating as cytokine storms that have far-reaching consequences for multiple organ systems, including the brain. ’

❦ Cognitive processing speed

The rate at which your brain takes in , interprets , and responds to information .

It is a crucial cognitive skill that affects how quickly you can understand instructions , solve problems , and complete tasks .

�� (4 Apr 2023 ~ EurekAlert / Journal of Alzheimer’s Disease Reports) New study shows SARS-CoV-2 infection accelerates the progression of dementia ➲

‘ All subtypes of dementia, irrespective of patients’ previous dementia types, behaved like rapidly progressive dementia following [ infection with SARS-CoV-2 ] .

The characteristics of a particular type of dementia changed following COVID-19, and both degenerative and vascular dementias started behaving like mixed dementia both clinically and radiologically.

A rapidly and aggressively deteriorating course was observed in patients having insidious onset, slowly progressive dementia, and who were previously cognitively stable.

Cortical atrophy was also evident in the study’s subsequent follow-ups.

Coagulopathy involving small vessels and inflammation, which were further correlated with white matter intensity changes in the brain, was considered the most important pathogenetic indicator.

The rapid progression of dementia, the addition of further impairments / deterioration of cognitive abilities, and the increase or new appearance of white matter lesions, suggest that previously compromised brains have little defense to withstand a new insult (i.e. a ‘second-hit’-like [ SARS-CoV-2 ] [ re ] infection). ’

Now consider a third, fourth, fifth and sixth-plus ‘hit’.

�� (5 Jul 2023 ~ The Lancet Regional Health: Western Pacific) Post-COVID cognitive dysfunction: current status and research recommendations for high risk population ➤

‘ Non-severe COVID-19 [ SARS-2 ] was associated with a [ 71% ] higher risk of early-onset cognitive decline , with an OR of 1.71 (1.30–2.27).

The increased risk of cognitive impairment , seizures , dementia , psychosis , and other neurocognitive conditions persisted for at least two years . ’

�� (17 Aug 2024 ~ Journal of Neuroinflammation) Deterioration of neuroimmune homeostasis in Alzheimer’s Disease patients who survive a COVID-19 infection ➤

‘ Our data demonstrate a profound impact of COVID-19 infection on neuroimmune and glial pathways in Alzheimer’s Disease patients persisting for months post-infection . ’

�� (28 Jul 2021 ~ Neurodegenerative Disease Management) Direct and indirect impact of SARS-CoV-2 on the brain ➤

‘ COVID-19 represents a credible risk for cognitive decline and has the potential to exacerbate pre-existing dementia .

For those at higher-baseline dementia risk, older adults, those with cardiovascular risk factors, and people of color, COVID-19 may not only increase the risk of cognitive decline but also interact in a synergistic way with pre-existing dementia risk factors to disproportionately increase this dementia risk . ’

�� (30 Aug 2021 ~ Canadian Medical Association Journal) Even mild COVID-19 may have long-term brain impacts ➤

‘ Research presented at the Alzheimer’s Association International Conference suggests even mild cases of COVID-19 may be associated with cognitive deficits months after recovery [ from the acute phase ] .

One Argentinian study of 234 seniors who previously had COVID-19 found that more than half showed some degree of cognitive impairment months later .

One in three had severe “dementia-like” impairments in memory , attention and executive function – a much higher proportion than the 5%–8% of seniors in the general population who have dementia at a given time.

Similar deficits have also been noted in patients after recovery from other coronaviruses . A 2020 systematic review and meta-analysis found that delirium was common in the acute stage of Severe Acute Respiratory Syndrome ( SARS ), Middle East Respiratory Syndrome ( MERS ), and COVID-19 [ SARS-2 ] .

Following up with patients six weeks to 39 months later , more than 15% reported sleep disorders , mood swings , trouble concentrating , impaired memory , and other mental challenges . ’

�� (17 Apr 2025 ~ Discover Mental Health) COVID-19 and cognitive impairment: a review of the emerging evidence ➤

‘ The acute phase of COVID-19 [ SARS-2 ] is marked by a rapid-onset inflammatory response that results in widespread neuronal damage and cerebrovascular complications .

In some cases, these acute insults resolve with time, leading to cognitive recovery.

However, for individuals with long COVID [ PASC ] , prolonged neuroinflammatory activity , persistent endothelial dysfunction , and sustained HPA axis dysregulation * contribute to chronic cognitive impairment . ’

* HPA axis dysregulation occurs when the communication between the hypothalamus , pituitary gland , and adrenal glands becomes disrupted , leading to abnormal cortisol levels and stress responses. This can result in symptoms like chronic stress , fatigue , mood instability , and various health issues .

❦ The cerebrum is the uppermost and largest part of the brain. It processes sensation , generates thought , and controls conscious activity .

The cerebrum has two sides – the right and the left hemispheres that each control the opposite side of the body – and each side is divided into four lobes with specific functions: the frontal lobe, the parietal lobe, the temporal lobe, and the occipital lobe.

❦ Frontal Lobe

The frontal lobe is responsible for higher executive functions like regulating emotions , planning , reasoning , and problem-solving .

❦ Parietal Lobe

The parietal lobe is responsible for processing and interpreting sensory information like touch , temperature , pressure , and pain . It is also involved in telling right from left , navigation , language , and reading .

❦ Temporal Lobe

The temporal lobe is responsible for hearing and understanding what we’re hearing , visual processing like recognising people’s faces, and memory .

❦ Occipital Lobe

The occipital lobe is responsible for sight and activities like reading and recognising colors .

❦ Cerebellum

The cerebellum is mainly responsible for balance , co-ordination , movement , and fine motor skills .

❦ Brainstem

The brainstem controls involuntary and essential functions such as breathing , and the beating of the heart .

❦ Meninges

The meninges are three layers of tissue that surround and protect the brain and the spinal cord . The meninges provide a support system and protect the nervous system from injury .

❦ Pituitary Gland

While not technically part of the brain, the pituitary gland secretes hormones and helps regulate many processes in the body like growth , metabolism , and reproduction .

�� (1 Apr 2023 ~ Human Genetics) Direct and indirect impact of SARS-CoV-2 on the brain ➤

‘ From mild anosmia to severe ischemic stroke , the impact of SARS-CoV-2 on the central nervous system is still a great challenge to scientists and healthcare practitioners.

Strikingly, even asymptomatic and mild-diseased patients may evolve with important neurological and psychiatric symptoms such as confusion , memory loss , cognitive decline and chronic fatigue , associated or not with anxiety and depression . ’

❦ SARS-CoV-2 (COVID-19) infections can lead to significant short- and long-term ( acute / chronic ) health effects in nearly every organ system of the body.

✺ Long Covid (LC)

Patient-coined term (2020).

✺ Post-Acute Sequelae of COVID-19 (PASC)

ICD-10 (International Classification of Diseases) code for PASC , commonly referred to as long COVID , is U09.9 (‘Post COVID-19 condition, unspecified’) (2021).

Annotations by C19.Life (2025). ➲

✾

Studies, articles & comment on... SARS-2, brain damage, neurological damage, and dementia

More ☰ Lists...

📖 Neurological and neurodevelopmental effects of Covid and MIS-C on children

Tue, 11 Nov 2025 16:59:54 GMT

‘The pediatric population, once thought to be relatively spared from severe outcomes, has presented with significant neurological manifestations that raise concerns about the short- and long-term effects of SARS-CoV-2 on the developing nervous system.’

✾

�� (11 Nov 2025 ~ Nature Pediatric Research) Neurological and neurodevelopmental effects of Covid and MIS-C on children ➤

[Layperson overview] �� (12 Nov 2025 ~ Bioengineer) Neurological Impacts of COVID and MIS-C in Children ➤

✾

❦ Scientific Media Article ~ Neurological Impacts of COVID and MIS-C in Children

❦ Layperson overview.

‘The emerging landscape of COVID-19 has revealed a stark contrast in how the virus manifests across different age groups, particularly highlighting a unique and alarming phenotype in children.

Unlike adults, the pediatric population infected with Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has shown susceptibility to distinctive inflammatory syndromes that were previously uncharacterized before the pandemic.

Chief among these conditions are Multisystem Inflammatory Syndrome in Children ( MIS-C ) and Pediatric Inflammatory Multisystem Syndrome Temporally Associated with SARS-CoV-2 ( PIMS-TS ), both of which have redefined the clinical understanding of pediatric COVID-19 and its complications.

While the respiratory symptoms of COVID-19 have dominated the early narratives of the disease, it has become increasingly clear that the virus’s impact stretches far beyond the lungs.

The pediatric population , once thought to be relatively spared from severe outcomes, has presented with significant neurological manifestations that raise concerns about the short- and long-term effects of SARS-CoV-2 on the developing nervous system.

These neurological symptoms range from subtle cognitive disturbances to severe inflammatory processes that affect brain function , reflecting a complex neurobiological response to viral infection and the host immune reaction.

The neurodevelopmental consequences of both acute COVID-19 infection and post-infectious inflammatory syndromes such as MIS-C/PIMS-TS in children remain critically underexplored.

A growing body of evidence indicates the nervous system’s vulnerability during critical periods of brain development, especially when confronted with systemic inflammatory insults triggered by SARS-CoV-2.

This points to a potentially troubling legacy of the pandemic – neurological sequelae that could impair children’s cognitive outcomes and quality of life long after recovery from the initial infection .

At the molecular level, the pathophysiology underlying SARS-CoV-2 neurovirulence is intricate and multifactorial.

The virus’s ability to engage receptors such as angiotensin-converting enzyme 2 (ACE2), expressed not only on respiratory epithelial cells but also on neurons and glial cells, hints at direct neuroinvasion routes.

However, much of the neurodamage observed in pediatric cases appears to be driven not solely by viral replication within neural tissue, but also by dysregulated immune responses causing widespread neuroinflammation and endothelial dysfunction , ultimately leading to blood-brain barrier disruption and neuronal injury .

Immunopathology plays a pivotal role in this context.

The cytokine storm triggered during MIS-C/PIMS-TS unleashes a barrage of pro-inflammatory mediators, elevating levels of interleukins and tumor necrosis factors that infiltrate the central nervous system (CNS), thereby precipitating encephalopathy , seizures , and other neurological symptoms .

Despite the growing recognition of these neurological effects , epidemiological data remain scant and fragmented. Current studies report variable prevalence of CNS * symptoms among children with COVID-19, with manifestations including headaches , encephalitis , neuropsychiatric disturbances , and peripheral neuropathies .

* CNS = Central Nervous System .

The heterogeneity of these presentations complicates early diagnosis and obscures the long-term prognosis, underscoring the urgent need for comprehensive, longitudinal research to delineate the full spectrum of neurologic sequelae.

From a clinical perspective, the management of these pediatric neurological complications demands multi-disciplinary approaches involving neurologists , immunologists , and critical care specialists .

The potential long-term neurodevelopmental impact of COVID-19 and related inflammatory syndromes represents a public health concern of unprecedented scale .

The developing brain’s plasticity and vulnerability necessitate follow-up strategies embracing neuropsychological assessments, educational support, and rehabilitative services tailored to individual needs.

Moreover, insights into the virus-derived neurotoxicity may inform preventative measures , including vaccination strategies optimized for children .

At the research frontier, unraveling SARS-CoV-2’s neuropathogenic mechanisms is paramount.

Concurrently, public health messaging must incorporate updated scientific knowledge regarding pediatric COVID-19 neurological risks, combating misinformation and fostering community awareness .

Empowering care-givers and healthcare providers with this information facilitates earlier recognition of symptoms, timely medical attention, and adherence to protective measures reducing exposure among children.

Impressively, vaccine campaigns have influenced the trajectory of pediatric COVID-19 outcomes, yet concerns persist regarding vaccine efficacy against emerging variants and their role in preventing MIS-C and neuroinflammatory complications.

Consequently, continuous vaccine safety monitoring and efficacy studies in children remain integral to controlling the neuropsychological burden attributed to SARS-CoV-2.

In conclusion, the neurological and neurodevelopmental aftermath of SARS-CoV-2 infection and its associated inflammatory syndromes pose complex challenges for pediatric health.

Comprehensive research efforts , coupled with proactive clinical and public health strategies , are essential for unraveling and mitigating the neurobiological consequences that may shape a generation of young survivors.

As science continues to illuminate this enigmatic facet of COVID-19, the imperative to safeguard the developing brain becomes ever more critical.’

✾

�� (12 Nov 2025 ~ Bioengineer) Neurological Impacts of COVID and MIS-C in Children ➤

✾

�� (11 Nov 2025 ~ Nature Pediatric Research) Neurological and neurodevelopmental effects of Covid and MIS-C on children ➤

✾

More... On SARS-CoV-2, children and babies

More... On SARS-CoV-2 and the neurological system

Knock-knock... It’s mild!

Wed, 05 Nov 2025 21:10:06 GMT

“How mild can a disease be?”

A copycat tale of mildness, taste, Public Health, and SARS-2.

✾

Learn Real Mildness ... it’s easy

‘Just make your next pack Chesterfields, that’s all, and as quick as you can light up, you’ll learn the meaning of real mildness...’

Chesterfield – THEY SATISFY

Mildness is a Pleasure with Pall Mall

‘Don’t miss the fun of smoking...

For flavor and enjoyment you just can’t beat Pall Mall’s natural mildness . It’s so good to your taste. Never too strong. Never too weak. Always just right!’

Outstanding... and they are Mild!

How mild can a cigarette be?

‘In a recent coast-to-coast test, hundreds of men and women smoked Camels – and only Camels – for 30 consecutive days .

These people smoked on the average of one to two packs a day .

Each week, during the entire test period, throat specialists examined those Camel smokers. A total of 2470 careful examinations were made.

The doctors who made the throat examinations of these Camel smokers reported :

“ NOT ONE SINGLE CASE OF THROAT IRRITATION due to smoking CAMELS! ”

According to a Nationwide survey:

MORE DOCTORS SMOKE CAMELS than any other cigarette

Doctors smoke for pleasure, too! And when three leading independent research organizations asked 113,597 doctors what cigarettes they smoked, the brand named most was Camel!’

Money-Back Guarantee!

Extra Special . Extra Mild .

‘Enjoy the great taste of Rothmans in a special mild cigarette.’

Warning : Health and Welfare Canada advises the danger to health increases with amount smoked – avoid inhaling.

Mild . But not Meek .

‘Mild, yes, because they’re lowered tar. But not meek, because they’re Raleigh.’

Warning : The Surgeon General Has Determined That Cigarette Smoking is Dangerous To Your Health.

“ GIVE YOUR THROAT A VACATION ~ Smoke a FRESH cigarette .”

‘If the cigarette you have been smoking stings or burns your throat , switch to Camels and see the difference.

It’s the peppery dust left in tobacco by inefficient cleaning methods that makes you cough .

It’s the unkindly hot smoke of harsh, dried-out tobacco that burns and irritates your throat .

There is no peppery dust in Camels – that’s whisked away by a special vacuum-cleaning process .

There are no stale, crumbly, parched tobaccos – the fine Turkish and mild Domestic tobaccos of which Camels are blended come to you in prime, factory-fresh condition, thanks to the Humidor Pack .

This scientific germ-safe wrapping – not plain ordinary Cellophane, but moisture-proof Cellophane which costs nearly twice as much – seals in all the natural aroma and freshness, seals it so tightly that wet weather cannot make Camels damp, nor drought weather make them dry.

Camels are milder and more throat-friendly because they are dust-free and fresh .

Give your throat a vacation, switch to Camels for just one day. Then leave them – if you can.’

Mild ... No Cigaretty After-Taste .

NEW ! CAMEL MILD INTERNATIONAL

Tar 9 mg, Nicotine 0,8 mg.

IT’S CHESTERFIELD

‘...for Real Smoking Pleasure it’s Chesterfield’s Milder, Better Taste every time.’

MILDNESS and BETTER TASTE

DANGER ... Aunt Nellie’s UPSTAIRS!

‘The Zeros started to dive. “I was a pigeon,” Sharkey said later. Visibility unlimited... no cloud-cover to hide in. He could not try to shoot it out with the Nips, because the transport carries no guns for fighting back. It’s dive – or else! And transports aren’t meant for diving...’

COLORS OF THE DAY

Thanks to the Chemical Warfare Service, G.I. Joe now talks in a new battle language – in color .

‘Using colored smoke grenades in code combination, Charlie signals exact target location to air support above.

“No job for a color-blind guy. Hey! There comes one of our A-20’s down for a look!”’

The Service First ~ CAMELS ~ First in the Service

NOW... Scientific Evidence on Effects of Smoking!

“Believe me, folks, you’ll want to read this important new evidence on the effects of smoking. Then you’ll say, as I do... MUCH MILDER! CHESTERFIELD IS BEST FOR ME! ”

‘ A MEDICAL SPECIALIST is making regular bi-monthly examinations of a group of people from various walks of life. 45 percent of this group have smoked Chesterfield for an average of over ten years .

After ten months, the medical specialist reports that he observed... no adverse effects on the nose , throat and sinuses of the group from smoking Chesterfield .’

MUCH MILDER ~ CHESTERFIELD IS BEST FOR YOU

RAMESES Modern Mildness

‘Rameses Modern Mildness is today’s most pleasing cigarette quality.’

The Aristocrat of Cigarettes for Half a Century

MILLIONS MUST AGREE – BECAUSE CAMEL LEADS ALL OTHER BRANDS!

‘Smokers all over the country have made the sniff test , the puff test – and the thorough 30-day Camel test to find out the score on cigarette mildness.

Now, after all the mildness tests, the smoke has cleared and Camel has its biggest lead in popularity in 25 years! The latest published figures show that Camel leads all other brands by billions of cigarettes !

Joan Crawford made her own 30-day Camel test – and compared for mildness and flavor. So have many other smokers.

Start your own sensible 30-day Camel test today. Enjoy Camel’s rich, full flavor – a flavor no other cigarette has. And see just how mild a cigarette can be – pack after pack , week after week! ’

‘TV STAR PHIL SILVERS KNOWS: PLEASURE HELPS YOUR DISPOSITION – IT’S A PSYCHOLOGICAL FACT!’

No other cigarette tastes so rich , yet smokes so mild .

The TAREYTON Twosome

‘Filter Tip Tareyton smokes milder , smokes smoother , draws easier . And Tareyton’s filter is pearl-gray because it contains Activated Charcoal for real filtration . It’s the best in filtered smoking!’

Only FILTER TIP TAREYTON gives you Activated Charcoal filtration

Spend a milder moment with Raleigh

‘A special treatment softens the tobaccos for a smoother, milder taste.’

For a TREAT instead of a TREATMENT...

‘No medical war whoops from Old Gold... We’re Tobacco Men , not Medicine Men! ’

‘No heap big medicine talk ... Old Gold cures just one thing: The World’s Best Tobacco.’

...smoke Old Golds .

MEDICAL AUTHORITIES RECOGNIZE PHILIP MORRIS proved far less irritating to the smoker’s nose and throat!

‘ DO YOU INHALE? All smokers do – sometimes. And when you inhale, there’s added chance of irritation.

So – choose your cigarettes with care!

Eminent doctors long ago reported that, compared with the strikingly contrasted Philip Morris: four other leading cigarettes were found to average 235% more irritant – with irritant effects lasting more than five times as long! *

* As reported in leading medical journals.

Our ads neither coax nor hoax – YOU DON’T find personal opinions ... private research ... high-pressure claims ... or special pleading ... in ads for Philip Morris cigarettes.

Claims or pleas look silly against this vital, proved difference. Reported by eminent doctors – in medical journals .

Their own findings that: When smokers changed to Philip Morris, every case of irritation of the nose and throat – due to smoking – cleared up completely , or definitely improved ! Actual men and women smokers, mind you – not laboratory “analysis” .

Proof that PHILIP MORRIS are far less irritating to your nose and throat.

NOTE : we do not claim curative power for PHILIP MORRIS. But, man! What solid proof they’re better ... safer ... to smoke! And do they taste GOOD! ’

PICTURE OF PERFECT SMOKING PLEASURE without smoking penalties .

Guard Against Throat-Scratch

Study this Puff Chart: PUFF BY PUFF YOU’RE ALWAYS AHEAD WITH PALL MALL

‘PALL MALL’s greater length of fine tobaccos travels the smoke further... filters the smoke and makes it mild. Here’s mildness you can measure.’

Outstanding... and they are MILD!

DO YOU THINK YOU ARE SMOKING TOO MUCH?

‘Then here, at last, is the cigarette especially blended for you !

Embassy gives you all the satisfying character, all the full-bodied flavor you enjoy in your present brand.

Yet, one of America’s leading research laboratories reports milder Embassy smoke averaged over 60% less Acid-Tars than that of 4 leading brands tested, when smoked the same normal length.

This amazing result indicates you get virtually no more Acid-Tars in three Embassys than in one ordinary cigarette!

So... if you think you are smoking too much... give Embassys a try.

You’ll find that your last cigarette of the day will taste as fresh and pleasant as your first !

Now... Inhale to your heart’s content! ’

Over 60% less Acid-Tars than that of 4 leading brands tested!

SILVA THIN ~ THE ONE THAT’S IN

‘Silva Thins 100’s have less “tar” than other Thins, even less than most Kings. But even better: Silva Thins have taste.’

SILVA THIN ~ THE ONE THAT’S THIN AND RICH

Latest U.S. Government figures show Silva Thins lowest in tar and nicotine of all 100’s.

THE SLIMMEST SLIM IN TOWN

CAPRI

SURGEON GENERAL’S WARNING: Cigarette Smoke Contains Carbon Monoxide

SURGEON GENERAL’S WARNING: Quitting Smoking Now Greatly Reduces Serious Risks to Your Health

SURGEON GENERAL’S WARNING: Smoking By Pregnant Women May Result in Fetal Injury, Premature Birth, And Low Birth Weight

Be Happy ~ Go Lucky!

‘L.S./M.F.T. ~ Lucky Strike Means Fine Tobacco.’

CAPRI

Regular, 9 mg. “tar”, 0.8 mg. nicotine.

av. per cigarette by FTC method.

the slimmest slim!

SURGEON GENERAL’S WARNING: Smoking Causes Lung Cancer, Heart Disease, Emphysema, and May Complicate Pregnancy.

SURGEON GENERAL’S WARNING: Smoking By Pregnant Women May Result in Fetal Injury, Premature Birth, And Low Birth Weight.

SURGEON GENERAL’S WARNING: Quitting Smoking Now Greatly Reduces Serious Risks to Your Health.

SURGEON GENERAL’S WARNING: Cigarette Smoke Contains Carbon Monoxide.

“DO YOU INHALE?”

“Certainly...”

“What’s there to be afraid of?”

“Everybody’s doing it!”

‘... wonder why cigarette advertising generally avoids this question?

One of the mysteries in cigarette advertising has been the apparent fear of the word “inhale” .

It seems rather foolish – for everybody inhales – whether they realize it or not... every smoker breathes in some part of the smoke he or she draws out of the cigarette.

Think, then, how important it is to be certain that your cigarette smoke is pure and clean – to be sure that you don’t inhale certain impurities.

Do you inhale?

Lucky Strike has dared to raise this vital question... because when you smoke Luckies your delicate membranes get the protection no other cigarette affords.

All other methods have been made old-fashioned by Luckies’ famous purifying process . Luckies created that process. Only Luckies have it!

Do you inhale? Of course you do! So truly this message is for you.’

7 out of 10 smokers inhale knowingly... the other 3 inhale unknowingly!

“It’s toasted . ”

“I discovered the smooth taste.”

‘Our unique charcoal filter smooths the smoke without thinning the taste.’

Av. per cigarette: Regular: 7.0mg “tar” 0.6mg nicotine.

Belmont Milds

Warning: Health and Welfare Canada advises that danger to health increases with amount smoked – avoid inhaling.

For people with a taste for something milder .

Av. per cigarette: 100 mm: 14 mg “tar”, 1.0 mg nicotine. King Size: 13 mg “tar”, 0.9 nicotine.

Warning: Health and Welfare Canada advises that danger to health increases with amount smoked – avoid inhaling.

Virginia Slims

‘In the new crush-proof purse pack.’

9 mg “tar”, 0.7 mg nicotine, av. per cigarette by FTC method.

You’ve come a long way, baby .

Warning: The Surgeon General Has Determined That Cigarette Smoking Is Dangerous to Your Health.

This is L&M – super bad

‘That show was out-of-sight.

You can still feel every note.

They played hot and hard.

They gave you the truth.

And now

you’re both ripe for L&M.’

‘The bold earth colors

of Africa right here at home.

A happy reminder

of roots to be proud of.

The very thought turns you

on to a real good feeling.

And now

you’re both ripe for L&M.’

‘Her pad.

Ribs and a good rap

topped off with a sweet

potato pie and coffee –

you can’t take another bite.

And now

you’re both ripe for L&M.’

Ah, the taste of an L&M Super King – super bad .

Warning: The Surgeon General Has Determined That Cigarette Smoking Is Dangerous to Your Health.

‘Hospital-Admitted Patient Care Activity: England.’

Chart data: Apr 2013 / 2014 to Apr 2025 :

❂ Mixed lung conditions , age 0-70+.

Chart data accessed : 23 October 2025 .

❂ To inspect/enlarge image: Right-click on image and ‘Open image in new tab’ .

Modern Mildness

‘The aristocrat of airborne diseases: Because Omicron is Mild.’

All the Gentleness of SARS-2 – Wrapped up in One, Simple Virion

Covid Omicron ® 2021 –

Modern Mildness

‘The aristocrat of airborne diseases: Because Omicron is Mild.’

All the Gentleness of SARS-2 – Wrapped up in One, Simple Virion

Covid Omicron ® 2021 –

❦ Catch up on your Omicron: A WHO’s Who of VOCs, VOIs and VUMs: Alphabet Stew and Numeric Ragout for Dummies ➲

‘Estimated cumulative excess deaths during COVID-19, World.’

From 1 Jan 2020 to 10 June 2024 :

❂ Lower bound , excess deaths: 19.24 million people.

❂ Central estimate , excess deaths: 27.27 million people.

❂ Upper bound , excess deaths: 36.29 million people.

Since 17 June 2024 : Zero ( 0 ) excess deaths.

❂ Confirmed COVID-19 deaths: 7.05 million people.

Chart data accessed : 25 September 2025 .

✾

More... Smoke, mirrors and mild propaganda

❦ Paper of interest:

�� The Doctors’ Choice Is America’s Choice – The Physician in US Cigarette Advertisements, 1930–1953

(American Journal of Public Health: Feb 2006)

A WHO’s Who of VOCs, VOIs and VUMs: Alphabet Stew and Numeric Ragout for Dummies

Sat, 01 Nov 2025 16:43:00 GMT

“We’re going to need a bigger Greek alphabet.”

✾

‘Omicron’ variants during the ‘Omicron Era’ (late 2021–): BA.1, BA.2, BA.4, BA.5, BA.2.12.1, BA.2.75, BQ.1, XBB, XBB.1.5, XBB.1.16, CH.1.1, XBB.1.9, XBB.2.3, EG.5.1, XBB.1.5.70, HK.3, BA.2.86, JN.1, JN.1.11.1, KP.3, XDV.1, KP.3.1.1, XEC, KP.2.3, LF.7, MV.1, LP.8.1, NB.1.8.1, and ‘Omicron’ XFG as of September 2025.

❦ A tale of Greek letters, variant stews, the WHO, and you

From May 2021 onwards , the World Health Organization ( WHO ) began to assign ‘ simple, easy-to-say-and-remember ’ labels for key SARS-CoV-2 Variants Of Concern ( VOC s) and Variants Of Interest ( VOI s), using letters of the Greek alphabet .

In March 2023 , the WHO abandoned this idea , announcing that Greek letters would only be assigned to major VOCs – while the lesser VOIs would be referred to using their scientific names (e.g. XBB.1.5/23A) – despite these names being ‘ difficult to say and recall... and prone to misreporting ’ (WHO ~ 31 May 2021).

In March of 2023 , the WHO also changed their working definitions for a Variant of Concern (VOC) and a Variant of Interest (VOI) , and added a brand new nebulous term into the mix – the ‘Variant Under Monitoring’ ( VUM ) – effectively ensuring that Omicron , now firmly cemented into the public’s consciousness as ‘mild’ and only a minor threat to human life, would remain synonymous with Covid infections for the foreseeable future.

No matter that Omicron had already made a quantum leap into unprecedented transmissibility by largely evading previous vaccines and dodging the protection of prior infections . The WHO’s new pot pourri of variant definitions also effectively buried any onward public panic over an aggressively neuroinvasive , immune- and cardiovascular-system-crashing Pi and Rho while not crashing the needles of the NASDAQ.

Confused? Good. All is explained by the WHO in this clear-as-mud , off-the-beaten-trail PDF download .

Compliant? Good.

Bored to the point of learned helplessness yet, dear reader?

Good.

The only thing you need not know is that the people dying around you of mildness while simultaneously living their best lives are, in fact, just getting repeatedly infected and beaten about the head by multiple strains of a neurotropic, highly vasculopathic SARS-CoV-2 variant formerly known as B.1.1.529 , now publicly celebrated as Eternal Omicron Mild [ ™ ] .

It’s not that hard to understand.

The WHO knew that they were going to run out of Greek letters by the end of 2022. The virus wasn’t just mutating at lightning speed, having out-stripped attempts at blocking it with a durable preventive vaccine . It had changed its game-plan, leaving the initial, dramatic ARDS far behind in the rear-view mirror of overflowing-hospital car-park headlines and desperate headcounts, and re-aimed itself fully at the nervous system, the immune system and the heart * – three of its primary objectives from the start.

* More specifically, ‘ vasculature ’ = the network of blood vessels in the body, or in a specific organ.

So in reply, the WHO didn’t just change the rules of their Letters game by making the new variant goalposts too small for any future VOC football to fit into: they changed the name of their game, too, and called slow death ‘Mild’.

Less a child picking up their ball and walking off the pitch; more a First Division manager (and his sponsors) folding up their astroturf, goalposts and all, and unrolling it in some Godforsaken desert in Central Asia where no-one will witness the final score of the game.

✾

‘Estimated cumulative excess deaths during COVID-19, World.’

From 1 Jan 2020 to 10 June 2024 :

❂ Lower bound , excess deaths: 19.24 million people.

❂ Central estimate , excess deaths: 27.27 million people.

❂ Upper bound , excess deaths: 36.29 million people.

Since 17 June 2024 : Zero ( 0 ) excess deaths.

❂ Confirmed COVID-19 deaths: 7.05 million people.

Data source : The Economist (2024); World Health Organization (2025).

Accessed : 25 September 2025 .

❦

❦ The Numbers Game, a year on ( 4 Nov 2025 ).

PE.1.4 is now a descendant of KP.3.1.1 .

To be clear:

PE.1.4 = MC.10.2.1.1.4 = KP.3.1.1.10.2.1.1.4 = Omicron B.1.1.529.2.86.1.1.11.1.3.1.1.10.2.1.1.4 .

➲ From ‘Genomic Mapping of SARS-CoV-2 / COVID-19 Variants’ by NextStrain.org / GISAID.org / C19.Life .

❦ Chart data accessed: 29 October 2024 .

✾

More... On naming conventions, the WHO, and SARS-CoV-2

More... Hype and Mirrors

On Biosafety Levels, Hazard Groups, SARS-CoV-2, the UKHSA, Notifiable Organisms and Notifiable Diseases

Thu, 23 Oct 2025 00:56:37 GMT

The Health and Safety Executive (HSE) has designated SARS-CoV-2, the virus that causes COVID-19, a Hazard Group 3 (HG3) pathogen that can cause severe human disease.

The United Kingdom’s Health Security Agency (UKHSA) classifies SARS-CoV-2 as a notifiable organism, and COVID-19 as a notifiable disease (2025).

✾

[ BSL ] Biosafety Levels 2, 3 & 4

➲ Biosafety Level 2 ( BSL-2 ) ~ Agents that can cause severe illness in humans.

BSL-2 pathogens include HIV , Zika virus , Hepatitis A , B & C , , Dengue , and Salmonella .

➲ Biosafety Level 3 ~ SARS-CoV-2 , the causative agent of COVID-19 , is a Biosafety Level 3 ( BSL-3 ) pathogen.

Other BSL-3 examples include the Yellow fever virus , West Nile virus , Yersinia pestis causing plague , and the bacterium Mycobacterium tuberculosis that causes tuberculosis ( TB ).

Biosafety Level 3 pathogens can cause serious or potentially lethal disease in humans.

➲ Biosafety Level 4 ( BSL-4 ) ~ The highest biosafety level.

Pathogens that pose a high risk of life-threatening disease for which there are no treatment s .

BSL-4 examples include the Ebola virus , Marburg virus , and Lassa virus .

✾

[ HSE ] ‘The Approved List of biological agents’

❦ ‘The approved list is for use by people who deliberately work with biological agents, especially those in research, development, teaching or diagnostic laboratories and industrial processes, or those who work with humans or animals who are (or are suspected to be ) infected with such an agent . ’ ➤

�� Health and Safety Executive (HSE) / Advisory Committee on Dangerous Pathogens: ‘The Approved List of biological agents’ (5th edition: 2023 ~ Accessed 23 Oct 2025) . [ PDF ] ➤

• Hazard Group 3 (HG3) definition : ‘Can cause severe human disease and may be a serious hazard to employees ; it may spread to the community , but there is usually effective prophylaxis or treatment available .’

• Severe-acute respiratory syndrome-related coronavirus 2 ( SARS-CoV-2 ) is a Hazard Group 3 biological agent . (p.28)

‘COSHH requires employers to control substances that are hazardous to health, including the protection of workers from risks related to exposure to biological agents at work.

This requires the UK to classify biological agents that are or may be a hazard to human health.’

[ Small print follows: feel free to scroll fast through this...]

‘The Health and Safety Executive has on 11 September 2023 approved the publication of this document, ‘The Approved List of biological agents’, for the purposes of the Control of Substances Hazardous to Health Regulations 2002 (SI 2002/2677).

This edition of the Approved List shall have effect from 11 September 2023. The Approved List will continue to be reviewed periodically.

The Advisory Committee on Dangerous Pathogens (ACDP) prepares the Approved List included in this publication. ACDP advises HSE, Ministers for the Department of Health and Social Care and the Department for the Environment, Food & Rural Affairs and their counterparts under devolution in Scotland, Wales & Northern Ireland, as required, on all aspects of hazards and risks to workers and others from exposure to pathogens.

This guidance is issued by the Health and Safety Executive.

Following the guidance is not compulsory, unless specifically stated, and you are free to take other action.

But if you do follow the guidance, you will normally be doing enough to comply with the law. Health and safety inspectors seek to secure compliance with the law and may refer to this guidance.

1. The Control of Substances Hazardous to Health Regulations 2002 (COSHH), make reference to the ‘approved classification’ of a biological agent, which is defined as the classification of that agent approved by HSE. The Approved List is the list of classifications of biological agents approved by HSE for this purpose. Biological agents are bacteria, viruses, parasites and fungi which can cause harm to human health, usually due to infection (some are toxic or can cause an allergy).

2. COSHH requires employers to control substances that are hazardous to health, including the protection of workers from risks related to exposure to biological agents at work. This requires the UK to classify biological agents that are or may be a hazard to human health.

‘ COSHH requires employers to control substances that are hazardous to health , including the protection of workers from risks related to exposure to biological agents at work .’

3. The Approved List is relevant to risk assessment for work with biological agents and the application of appropriate control measures. Your risk assessment under COSHH of work likely to expose any employees to biological agents should include consideration of the approved classification of any biological agent (regulation 6(2)(k)). The risk assessment must identify the steps you will take to adequately control exposure to biological agents (where it is not reasonably practicable to prevent exposure), taking into account the hazard(s) that they present (regulations 6 and 7).

4. The Approved List is intended to be used by people who work with biological agents, especially those in research, development, teaching or diagnostic laboratories and industrial processes, and people working with animals or humans who are, or who are suspected of being, infected with such an agent.

5. The classifications in the Approved List assign each biological agent listed to a hazard group according to its level of risk of infection to humans, where Hazard Group 1 agents are not considered to pose a risk to human health and Hazard Group 4 agents present the greatest risk. The full definition of each hazard group is in the Information Box (see page 9). Only agents in Groups 2, 3 and 4 are listed.

6. ACDP has made the relevant classification of a biological agent having considered evidence as to:

the likelihood that it will cause disease by infection or toxicity in humans;
how likely it is that the infection would spread to the community;
the availability of any prophylaxis or treatment.

7. The Approved List indicates in the taxonomy/notes column which biological agents are toxigenic or an allergen, or for which a vaccine was readily available at the time of publication.’

✾

Annex 1: Biological agents which may be used at less than the minimum containment conditions

Viruses [ complete list ]

Chikungunya virus
Everglades virus
Hepatitis B virus
Hepatitis C virus
Hepatitis D virus
Orthohepevirus A (formerly known as Hepatitis E virus)
Human immunodeficiency viruses
Primate T-cell Iymphotropic viruses
Louping ill virus
Mucambo virus
Rabies virus
Simian immunodeficiency virus
Tonate virus
Wesselsbron virus

✾

[ UKHSA ] ‘Notifiable diseases and how to report them’

( Accessed : 23 Oct 2025 ~ UK Health Security Agency) ‘Health surveillance and reporting programmes: Notifiable diseases and how to report them ’. ➤

‘ Registered medical practitioners must report a notifiable disease to the UK Health Security Agency ( UKHSA , previously Public Health England).

Do not wait for laboratory confirmation of the disease. By law , you must report any suspicion of a notifiable disease .’

➲ Diseases you must report

‘You must report any suspected case of a notifiable disease .

❂ Notifiable disease : COVID-19 .

❂ Whether likely to be routine or urgent : Routine .’

‘A case may be urgent if :

it’s part of a current outbreak ;

the suspected disease is uncommon in the UK;

the suspected disease spreads easily , or its spread is hard to control ;

the patient is high risk , for example because of their age or job .’

Published by UKHSA : 12 September 2024

Last updated : 29 April 2025

✾

[ UKHSA ] ‘Notifiable organisms and how to report them’

( Accessed : 23 Oct 2025 ~ UK Health Security Agency) ‘Health surveillance and reporting programmes: Notifiable organisms and how to report them ’. ➤

‘ All laboratories in England with a primary diagnostic role must report a confirmed notifiable organism to the UK Health Security Agency (UKHSA, previously Public Health England).’

➲ List of notifiable organisms (causative agents)

‘ Causative agents notifiable to UKHSA under the Health Protection (Notification) Regulations 2010:

❂ Notifiable organism (causative agent) : SARS-CoV-2 .

UKHSA publishes reports on the numbers of laboratory notifications received.

See Notifications of infectious diseases ( NOIDs ) and causative agents report .’ ➤

Published by UKHSA : 12 September 2024

Last updated : 11 August 2025

✾

[ Coping Strategies ] ‘Stop counting’

“How does Covid being a notifiable disease interact with the UK government discouraging testing?

How does this work?

How does it work with NHS Trusts telling their staff not to test?”

Tern, a priest in England (28 Aug 2023)

✾

[ Coping Strategies ] ‘Stop testing so you don’t need to report anything’

“If we didn’t do any testing, we would have very few cases.”

Donald John Trump (15 May 2020)

✾

( Accessed : 23 Oct 2025 ~ UK Health Security Agency) Health surveillance and reporting programmes ’. ➤

✾

“If we stop testing right now, we’d have very few cases, if any.”

Donald John Trump (15 June 2020)

✾

More... On Healthcare Workers

More on... COSHH

Solutions in... NHS Estates Bulletins

From... The UKHSA

More... Healthcare Worker insights

✾

📖 Guidance for Healthcare Employers and Workers on the use of Fluid Resistant Surgical Masks (FRSM) and respirators (FFP3 etc) to comply with the requirements of COSHH (2002) (England) (Updated 2025)

Mon, 20 Oct 2025 16:08:58 GMT

‘FRSMs [Surgical Masks] have never been considered either adequate or suitable equipment for protection against inhalable or respirable risks under COSHH.’

✾

‘Healthcare workers and employers will rightly focus on the safe and effective provision of patient care for patients.

This is the central concern of the Health and Social Care Act, which creates the architecture for IPC [ Infection Prevention and Control ] .

The central aim of this Act is to ensure that the environment is managed effectively to prevent the transmission of infections and that healthcare workers do not inadvertently act as agents for transmission, either because of insufficient hygiene precautions, or because they are themselves infected and could therefore infect others.

Biological hazards can be transmitted via an oral/faecal route, or bloodborne routes, by droplet, fluid splashes, airborne particles or any combination.

COSHH requires all possible routes of exposure to be controlled.

FRSMs [ Surgical Masks ] have never been considered either adequate or suitable equipment for protection against inhalable or respirable risks under COSHH.

The only respiratory protective equipment [ RPE ] designated as such for the protection against biological agents is the FFP3 or another respirator type with the same assigned protection factor (APF) (e.g. reusable ‘elastomeric’ respirators, or powered hoods with the appropriate filter).

Failure to comply with COSHH and control standards for RPE is a criminal offence.

This relates to:

(a) the employer’s duty to provide suitable RPE and ensure that it is properly used, inspected and maintained;

and (b) the employee’s duty to wear the RPE as instructed by the employer and to take reasonable care of it.’

✾

‘ COSHH and Healthcare Respiratory Protection: Guidance for Healthcare Employers and Workers on the use of Fluid Resistant Surgical Masks (Type IIR) and respirators (FFP3 etc) to comply with the requirements of the Control of Substances Hazardous to Health Regulations (COSHH) (2002) (England) (Updated 2025) .’

[ Abridged ] ‘COSHH and Healthcare Respiratory Protection’

‘ Respiratory infections have long been a recognised hazard of working within healthcare settings .

The principal concern of healthcare legislation and healthcare employers has been the protection of patients who are likely to be vulnerable to such infections, with precautions designed accordingly. ’

Page 1

‘ Equipment designed to protect the wearer against infection by inhalable pathogens is “ respiratory protective equipment ” ( RPE ), a type of personal protective equipment ( PPE ) designed to reduce ( or eliminate ) the risk of inhalation of infected particles .

Examples of RPE include FFP3 , FFP2 (and N95 [and N99 / N100 ]) respirators which work by the wearer of a respirator drawing in air through filters designed to remove infected particles from the air.’

Page 1

‘ If any control , whether through segregation, barrier controls, [or] ventilation, leaves any risk of exposure of an individual worker to a respiratory hazard , then so far as it is reasonably practicable, RPE must be provided and worn in line with health and safety regulations. ’

Page 2

‘ Training on duties in relation to respiratory protection and the management of RPE has not been widespread through the health service.

There has also been some confusion in Government bodies as to who has regulatory oversight of RPE in the health service as well as the applicable science.

In 2024 , the World Health Organisation (WHO) , recognising a global need for greater clarity, reviewed the approach to respiratory infection and control .

The new approach recommended by WHO has not been incorporated into UK IPC guidance but is entirely consistent with UK Health and Safety Law . ’

Page 3

‘ Healthcare workers and employers will rightly focus on the safe and effective provision of patient care for patients.

This is the central concern of the Health and Social Care Act , which creates the architecture for IPC .

The central aim of this Act is to ensure that the environment is managed effectively to prevent the transmission of infections and that healthcare workers do not inadvertently act as agents for transmission , either because of insufficient hygiene precautions , or because they are themselves infected and could therefore infect others . ’

Page 3

‘The overriding legal duty is to protect the health and safety of employees , as well as others for whom an undertaking will impact ( including patients , service users , contractors and visitors ).

Considerations should not be driven by whether someone has a patient-facing or clinical function, is an employee, is in one healthcare setting or another, but should be focused on the risk to that person of exposure to substances hazardous to their health ’

Page 4

‘ Patients and service users may be vulnerable to biological hazards that would not be a concern for a healthy person exposed to an infectious agent.

For this reason, quite rightly, there is a great emphasis placed on ensuring that healthcare workers do not become the inadvertent agents of the spread of pathogens . ’

Page 5

‘ Every effort should be made to exclude the pathogen from the place of work .

If this is not possible, engineered controls , not dependent on individuals for their effectiveness, should be deployed , e.g. negative pressure treatment areas or highly effective ventilation . ’

Page 6

‘ Biological hazards can be transmitted via an oral/faecal route, or bloodborne routes, by droplet, fluid splashes, airborne particles or any combination.

COSHH requires all possible routes of exposure to be controlled . ’

Page 6

‘ FRSM s [ Fluid Repellent Surgical Masks ] are, unhelpfully , described as Personal Protective Equipment in the NIPCM .

This is incorrect both in law and in practical terms .

This incorrect designation of FRSMs as PPE or RP E is commonplace within NHS literature and perpetuates a dangerous and illegal inaccuracy .

The only respiratory protective equipment designated as such for the protection against biological agents is the FFP3 or another respirator type with the same assigned protection factor (APF) (e.g. reusable ‘ elastomeric ’ respirators, or powered hoods with the appropriate filter). ’

Page 7

‘ FRSMs , as barriers, belong elsewhere in the hierarchy of controls when dealing with respiratory risk, because they do not provide adequate control to prevent the inhalation of infectious particles .

They are not designed to do so and to provide them for that purpose would be in breach of COSHH . ’

Page 8

‘ [ FRSMs’ / Surgical Masks’ ] effective performance in reducing infection by pathogens such as influenza , even in vitro testing by HSE, will seldom achieve beyond 40% .

Providing an employee with a device that only protects them to that level for a hazardous pathogen would be insufficient and there would be a requirement, in the absence of other highly effective controls, to also provide recognised RPE in order to be legally compliant . ’

Page 9

‘ FFP3s are made of complex filtering material designed to remove 99% of inhalable and respirable particles .

Of course, they only work as a filter if they are tightly fitted to the face , otherwise they cannot provide that extremely fine filtering as contaminated air will leak into the breathing space through gaps in the face seal . ’

Page 9

‘Where there is a risk of exposure of a worker to a significant respiratory hazard which cannot be controlled by other means, including the use of medical devices such as FRSMs, then adequate and suitable RPE must be provided .

Adequate RPE for biological agents is RPE designed to reduce exposure risk to as low as it is reasonably practicable to do so.

Thus, if there is a transmission route involving inhalable respiratory particles such as aerosols , even if a contact transmission route is predominant, then that risk has to be reduced by the use of an FFP3 or equivalent . ’

Page 10

‘If RPE fails to achieve the levels of protection it is designed to achieve in healthcare settings , then this is an indication of the failure of the employer to ensure that RPE has been correctly managed to ensure that it achieves its designed protective capability.

This is undoubtedly a breach of Health and Safety law . ’

Page 10

‘ FRSMs have never been considered either adequate or suitable equipment for protection against inhalable or respirable risks under COSHH . ’

Page 10

❦ ‘Guidance for Healthcare Employers and Workers on the use of Fluid Resistant Surgical Masks (Type IIR) and respirators (FFP3 etc) to comply with the requirements of the Control of Substances Hazardous to Health Regulations (COSHH) (2002) (England)’

By The British Occupational Hygiene Society (Updated by BOHS : 2025 / Accessed: 20 Oct 2025 )

[ Full document ] ‘COSHH and Healthcare Respiratory Protection’

Introduction

[ Long document ahead : feel free to scroll fast past this ...]

Respiratory infections have long been a recognised hazard of working within healthcare settings. The principal concern of healthcare legislation and healthcare employers has been the protection of patients who are likely to be vulnerable to such infections, with precautions designed accordingly.

Prior to the COVID-19 pandemic, regulators regarded instances of harm to healthcare workers from pathogens spread by the respiratory route of transmission (such as influenza, SARS coronaviruses, Respiratory Syncytial Virus [RSV] etc.) as having been relatively rare. This perspective requires revision as a result of the acute and long-term impact of COVID-19 on healthcare workers.

As a consequence of this, healthcare workers and their employers had a great degree of familiarity with medical devices designed to protect patients against respiratory infection by healthcare workers and, indeed, protective equipment designed to protect against contact, ingestion and bloodborne routes. However, awareness of controls to prevent respiratory infection of healthcare workers via the inhalation route has not been as widespread.

Medical devices designed to prevent the wearer from passing on infections to others are typically described as “source control,” because they restrict the source of infection by creating a barrier between the infected wearer and the sterile environment. These devices, like surgical masks, are not personally protective, but interrupt the transmission of infection by reducing the risk that an infected person will pass the infection by creating a barrier to reduce the number of particles, droplets and splashes they might release from their mouth and nose.

The COVID-19 pandemic was, understandably for many, the first time that they were required to deploy or use apparatus designed to protect healthcare workers themselves against inhalation of pathogens. Equipment designed to protect the wearer against infection by inhalable pathogens is “respiratory protective equipment” (RPE), a type of personal protective equipment (PPE) designed to reduce (or eliminate) the risk of inhalation of infected particles. Examples of RPE include FFP3, FFP2 (and N95) respirators which work by the wearer of a respirator drawing in air through filters designed to remove infected particles from the air, and powered filtering respirators which deliver filtered air to the wearer’s breathing zone via a hood.

Understandable confusion has developed between surgical masks (source control) and respirators (wearer personal protection). Both have a role in the reduction of infection prevention and control (IPC), both are worn on the face, both are termed as “PPE” in the National Infection Prevention and Control Manual (NIPCM) and both were recommended by Government and Healthcare Bodies for the control of transmission of COVID-19 at various times and in various places during the pandemic. However, each has a very different function and their use is directed as part of two different systems of legal obligations.

• Surgical masks are devices for use in furtherance of patient safety, as outlined by the Health and Social Care Act 2008. Failure to follow these duties may result in regulatory intervention against a healthcare provider by the Care Quality Commission in England and disciplinary action against a healthcare worker in breach.

• RPE is used to protect workers against infection in furtherance of duties under the Health and Safety at Work Act etc 1974. Breach of duties by an employer is a criminal offence, enforceable by the Health and Safety Executive. It is also a criminal offence for a worker not to comply with these duties and could also result in disciplinary action against a healthcare worker in breach.

The purpose of this guidance note is to ensure that employers and healthcare workers can have a clear understanding of the differences between medical devices used as source control, particularly surgical masks, and RPE, particularly filtering facepiece respirators used as wearer personal protection.

This guidance does not express opinions as to the suitability of each type of device to control specific risks arising from specific pathogens. However, it is a legal requirement in either case that, when determining the suitability of a device to provide control, reference is made to the manufacturer’s instructions. In addition, when using each type of device, scientific and technical guidance produced by the relevant regulator must be followed.

In practice this means that, when using surgical masks as source control (to protect the sterile environment), the Infection Prevention and Control Manual should be followed, as well as any technical and scientific guidance. When using RPE to protect the safety of the wearer, the HSE’s guidance should be followed, as well as any specific technical and scientific guidance.

The IPC regulatory regime is open to clinical interpretation and a wider range of professional discretion using dynamic risk assessment. However, once it has been determined that other methods cannot completely protect a worker against a substance hazardous to health, necessitating the use of RPE, the COSHH Regulations and accompanying official guidance and codes of practice should be followed.

The hierarchy of controls including segregation, ventilation etc is not, however, to be taken as being an order of priority or preference. If any control, whether through segregation, barrier controls, ventilation, leaves any risk of exposure of an individual worker to a respiratory hazard, then so far as it is reasonably practicable, RPE must be provided and worn in line with health and safety regulations. This is not a consideration that is made after the implementation of other controls and where there is evidence of actual control failure, but a decision that needs to be made at the stage of an initial risk assessment and the identification of practicable controls.

Thus, while good general ventilation and source controls such as masks may reduce respirable risk, these measures may not reduce the risk to individuals of inhaling hazardous infectious pathogens, e.g. at close quarters or where the infection is transmitted to some degree by smaller airborne droplets known as aerosols. Such a residual risk of infection, while reduced by other interventions higher up the hierarchy of controls, would require the use of RPE as part of the system of controls to meet the expected threshold under COSHH.

When considering the relative merits of surgical masks and RPE, the primary purpose of either type of device must not be overlooked. Surgical masks aim to contribute to a reduction in overall infections for patients and workers. Failures in adherence and the effectiveness of the device in achieving this is a regulatory performance issue.

Respirators protect the wearer against respiratory exposure to infective agents.

Training on duties in relation to respiratory protection and the management of RPE has not been widespread through the health service. There has also been some confusion in Government bodies as to who has regulatory oversight of RPE in the health service as well as the applicable science.

In 2024, the World Health Organisation (WHO), recognising a global need for greater clarity, reviewed the approach to respiratory infection and control. The new approach recommended by WHO has not been incorporated into UK IPC guidance but is entirely consistent with UK Health and Safety Law.

This guide aims to help employers and worker representatives with a clear statement to outline the differences between medical devices used in IPC (such as the Type IIR mask) on the one hand and RPE on the other. It aims to outline how compliance with IPC measures may not automatically equate to COSHH compliance. Similarly, compliance with COSHH may not necessarily meet IPC standards.

Legal Duties

Healthcare workers and employers will rightly focus on the safe and effective provision of patient care for patients. This is the central concern of the Health and Social Care Act, which creates the architecture for IPC. The central aim of this Act is to ensure that the environment is managed effectively to prevent the transmission of infections and that healthcare workers do not inadvertently act as agents for transmission, either because of insufficient hygiene precautions, or because they are themselves infected and could therefore infect others.

The Act sets out principled requirements for bodies inspectable by the Care Quality Commission Health and Social Care Act 2008: code of practice on the prevention and control of infections and related guidance - GOV.UK .

The Code states:

“However, the code is not mandatory so registered providers do not by law have to comply with the code. A registered provider may be able to demonstrate that it meets the regulations in a different way (equivalent or better) from that described in this document.”

It further states:

“The code does not replace the requirement to comply with any other legislation that applies to health and social care services; for example, the Health and Safety at Work Act 1974 and the Control of Substances Hazardous to Health Regulations 2002.”

All healthcare governance bodies, with responsibilities for guiding employees and patients, as well as employing organisations have legal duties under Health and Safety law. This arises, among other legal duties, in section 2 (1) of the Health and Safety at Work Act.

(1) It shall be the duty of every employer to ensure, so far as is reasonably practicable, the health, safety and welfare at work of all his employees.

Section 3(1) extends the duty to third parties.

Therefore, the following considerations should be kept in mind when formulating guidance, rules, training, protocols and procedures which have an impact on health and safety (as they relate to the use of surgical masks and respirators):

1) The overriding legal duty is to protect the health and safety of employees, as well as others for whom an undertaking will impact (including patients, service users, contractors and visitors);

2) Considerations should not be driven by whether someone has a patient-facing or clinical function, is an employee, is in one healthcare setting or another, but should be focused on the risk to that person of exposure to substances hazardous to their health;

3) Guidance which may be evidence-based in relation to the reduction of infectious risk, which uses administrative methods or medical devices to reduce risk, is a useful element of the hierarchy of controls. However, if there is a residual risk of workers being exposed to hazardous substances, then so far as reasonably practicable, approved RPE must be provided to eliminate that risk.

4) Terminologies, such as “PPE ensemble” and the casual description of medical devices, or fluid resistant surgical masks as “PPE”, should be avoided. Only equipment designed and tested as personal protective equipment, in line with the appropriate standards and which has been determined to adequately control the exposure and which is suitable for the wearer and their work, will be compliant with legal duties.

COSHH vs IPC

Keeping infectious agents out of healthcare areas is difficult. The historic challenges of controlling healthcare acquired infections have led to the current complex infrastructure to help ensure patient safety. Patients and service users may be vulnerable to biological hazards that would not be a concern for a healthy person exposed to an infectious agent.

For this reason, quite rightly, there is a great emphasis placed on ensuring that healthcare workers do not become the inadvertent agents of the spread of pathogens.

The governance and infrastructure of healthcare institutions in the UK is framed by this focus when it comes to IPC. In many contexts, by maintaining good IPC standards, for example sterile environments, good hygiene and the use of bespoke medical devices, healthcare workers will also be protected from exposure.

However, there should not be an automatic assumption that maintaining acceptable and practicable standards of IPC will meet the threshold for protecting workers from exposure as required by COSHH. Equally, standard PPE measures for the control of exposures to workers, such as the use of respirators with exhalation valves, which may compromise the health and safety of others, may need to be re-thought.

The inter-relationship between IPC practices and COSHH practices may seem confusing.

When considered in the context of other concepts, such as the hierarchy of controls, this confusion can escalate further. The use of the same terminology which means different things in two different regulatory systems can be even more confusing.

To explain further, consider this:

1) To prevent the transmission of a pathogen which may be very hazardous to a patient, but not unduly hazardous to a worker, there may be a range of options. It may be accepted that the nature of work that a person does, brings a high probability of infection because of the patients cared for or the role undertaken. If the worker is infected: they may be sent home; deployed away from dealing with certain high-risk patients; be provided with source control equipment (such as surgical masks); or may be immunised so that an infection does not develop in them that can be transmitted further. All of these approaches may be entirely lawful when considering the practicability of preventing exposure to infection.

However, all of these IPC measures still allow the healthcare worker to be infected. The exposure is entirely lawful in IPC terms and can be defensible in COSHH terms if the benefit of completely preventing exposure of the healthcare worker is greatly outweighed by the sacrifice the healthcare provider would have to make to protect the worker.

2) To prevent a pathogen which is directly hazardous to the worker as well as to patients, a different approach may be required. If exposing the worker to a pathogen may have serious and irreversible impact on their health, then the options outlined above would not be lawful.

Every effort should be made to exclude the pathogen from the place of work. If this is not possible, engineered controls, not dependent on individuals for their effectiveness, should be deployed, e.g. negative pressure treatment areas or highly effective ventilation. It would be relatively unusual for a designed solution such as this to work on its own, since compliance by healthcare workers with protocols, such as who is allowed into such a controlled area, need to be in place.

These “administrative controls” rely on compliance and people management.

Finally, however, there will be circumstances where a worker cannot benefit from the protection of the engineered control because, for example, they are providing close quarter care. In these instances, rather than controlling the environment or access to the environment, the focus on controlling the risk must be on protecting the person.

PPE is highly dependent on its correct selection, its correct use and management.

Importantly, the PPE must be suitable to meet the needs of the person, e.g. a person’s physical characteristics such as size and shape (also face size and shape with regard to face seal of FFPs) and the type of work that they do. The suitability of PPE requires a thorough risk assessment (as outlined in HSE guidance, for example), careful consideration, planning and analysis. What works for one person may not work for another. As well as being suitable, PPE needs to adequately protect the wearer so far as is reasonably practicable from the risk of hazardous exposure. This means that the device itself should be designed to be capable of providing a specified degree of protection (as defined in applicable UK designated standards).

It is therefore paramount that all the factors of how PPE may be compromised are considered and appropriately managed. In some ways, this is common sense. A firefighter may attend a fire and may be exposed to flames, fumes, oxygen deprivation, toxic dust, falling debris, heat exhaustion and a range of other risks.

When determining the appropriate PPE, all the potential risks need to be protected against so far as reasonably practicable. If the respirator protects against toxic dust but does not protect against oxygen deprivation, the hazard is not controlled.

The same applies to the control of infectious pathogens. Biological hazards can be transmitted via an oral/faecal route, or bloodborne routes, by droplet, fluid splashes, airborne particles or any combination.

COSHH requires all possible routes of exposure to be controlled. Thus, for infectious diseases, all possible routes of transmission need to be considered unless the level of risk being protected against is marginal compared to the sacrifice required to achieve adequate control. Thus, while a face visor may protect the mucosa from splashes and therefore control a deposition route to infection, it will not control the risk of inhalation of airborne pathogens which may cause infection.

Even if the predominant route of infection is by fluid splashes, if there is another transmission route (e.g. inhalation) and the pathogen is hazardous to health via inhalation, then infection via the inhalation route must also be adequately controlled. That is the legal requirement of COSHH. By contrast, from an IPC point of view, it may be viewed that infection transmission can be most effectively reduced by focusing on the predominant mode of transmission and using other measures, such as the removal of infected staff from the roster.

These differing approaches represent a fundamental difference in the tolerance of risk of infection of individual healthcare workers. The former focuses on the reduction of the risk of exposure for each worker so far as reasonably practicable, whereas the latter looks at the impact in overall infection transmission within the healthcare setting, often with a priority on the extent of patient risk, balanced against operational delivery.

FRSM vs FFP3

The COVID-19 pandemic and the COVID-19 Inquiry has brought into sharp contrast fundamental misunderstandings about IPC measures and COSHH measures. This is typified by ongoing debates about the relative roles of Type IIR Fluid Resistant Surgical Masks (FRSMs) and Filtering Facepiece Respirators - level 3 (FFP3s). Both devices have roles within both the achievement of IPC and COSHH outcomes, but in quite different ways.

Sometimes the debate is unhelpfully abbreviated to “masks” vs “respirators”. Even this simplification is fraught with danger. Conflating all masks together (whether or not they are fluid resistant) would be problematic. Similarly, conflating FFP1 (low level protection), FFP2/N95 (higher level protection) and FFP3 (or N99, the US equivalent of FFP3) is not helpful. Each provides a different level of filtration and consequent protection.

In WHO documentation, NHS research material and submissions to the COVID-19 Inquiry, evidence about the effectiveness of masks vs respirators which conflates these devices and equipment has caused confusion which undermines legal compliance.

FRSMs are, unhelpfully, described as Personal Protective Equipment in the NIPCM. This is incorrect both in law and in practical terms. This incorrect designation of FRSMs as PPE or RPE is commonplace within NHS literature and perpetuates a dangerous and illegal inaccuracy.

The only respiratory protective equipment designated as such for the protection against biological agents is the FFP3 or another respirator type with the same assigned protection factor (APF) (e.g. reusable ‘elastomeric’ respirators or powered hoods with the appropriate filter).

This is because, while both are worn about the face and both have a role in the prevention of infection, they are very different things. In very simple terms, these are the distinctions.

• FFP3s are designed and tested to filter respirable and inhaled particles (including viral and other pathogens). The whole device aims to protect the wearer from anything but the smallest level of exposure, provided it is selected and used correctly.

• FRSMs are designed and tested to create a barrier to exhaled bacteria in droplets and to be made of material which resists pressurised artificial blood. The effect is to reduce the risk of the wearer’s exhaled breath contaminating a sterile environment with bacteria. It also creates a barrier for the wearer against splash contamination by liquids around the nose and mouth, if worn correctly.

(From a technical and legal perspective, the differences are summarised below in Annex I.)

The differences between the underpinning design and operation of FRSM and FFP3 (a barrier and a filter; exhalation and inhalation; droplets containing bacteria and respirable viral particles such as aerosols; protecting others and protecting the wearer) must make it clear that these are two very different types of devices designed for two very different purposes.

In terms of IPC, the premise of an FRSM is that the wearer may be infected with a pathogen transmitted by larger droplets and that the barrier can protect against those droplets having an uninterrupted trajectory into a sterile environment or onto a patient.

They may also present a barrier to splashes and droplets that have a trajectory towards the wearer’s mouth and nose. In that respect, they operate almost the same as a visor barrier or screen. They can provide a vital break in human-human transmission probability, especially where there is a significant role for pathogen transmission by direct deposition of fluids in splashes or droplets.

This is a barrier method of protection, but anything that can circumvent the barrier, such as a particle suspended in the air, can compromise its role as a protective device. Inhaled respirable particles are therefore inherently capable of getting drawn in through the gaps between the mask and the wearer.

FRSMs are not tightly fitted to the face (and are not designed to be) because the fluid resistant material would also make breathing very difficult. The reason for the general requirement of fit testing of RPE is that leakages due to poor seals defeat the very fine filtration design.

FRSMs, as barriers, belong elsewhere in the hierarchy of controls when dealing with respiratory risk, because they do not provide adequate control to prevent the inhalation of infectious particles. They are not designed to do so and to provide them for that purpose would be in breach of COSHH. That does not mean that high mask adherence cannot reduce the risk of transmission of a pathogen which has a deposition transmission route.

However, their effective performance in reducing infection by pathogens such as influenza, even in vitro testing by HSE, will seldom achieve beyond 40%. Providing an employee with a device that only protects them to that level for a hazardous pathogen would be insufficient and there would be a requirement, in the absence of other highly effective controls, to also provide recognised RPE in order to be legally compliant.

FFP3s are made of complex filtering material designed to remove 99% of inhalable and respirable particles. Of course, they only work as a filter if they are tightly fitted to the face, otherwise they cannot provide that extremely fine filtering as contaminated air will leak into the breathing space through gaps in the face seal.

Many FFP3s are fitted with exhalation valves. This makes them largely unsuited to protecting the sterile environment against the risks posed by the wearer if they are infected with a pathogen which could be transmitted by fluids, direct deposition or condensates of respirable particles. Therefore, while valved FFPs protect the wearer from respiratory risk, they may not provide an effective IPC control, if the wearer is infected. Not all FFP3s will meet the impermeability standards for Type IIR FRSMs either, potentially presenting a risk for a fluid-based infection. If there is a risk of wicking of infectious fluid, then an FFP respirator with fluid resistant properties would be appropriate.

The very limited availability of unvalved FFP3 respirators, with fluid resistant properties, capable of achieving an effective fit to faces of healthcare workers during the pandemic reflected a failure to have a secure supply or stockpile of adequate (i.e. designed to achieve the right level of protection) and suitable (i.e. fits the person and works in the context of their activity) RPE. In the context of the pandemic, this lack of availability meant that it may not have in all circumstances been reasonably practicable to meet the standards expected in COSHH while those shortages persisted.

FFP3 respirators with certified fluid resistance (Type IIR), which are designed in vitro to filter 99% of respirable particles, were certified as an alternative to FRSMs to provide IPC control in the same way as FRSMs.

The preponderance of citations in NHS literature (as to the relative effectiveness of masks against respirators in the control of infection) are derived from overseas studies and almost exclusively consider comparisons with N95 filtering facepieces. N95 respirators are equivalent to FFP2 respirators in the UK, which would not be deemed to provide adequate control of respirable particles under UK law.

Clinical studies almost never record the extent to which face fit requirement for N95s has been implemented, meaning the deployment of respirators may not meet the UK’s standards for testing suitability of the equipment to the wearer.

The apparent lack of technical understanding of these fundamental RPE principles by reviewing authors means studies such as The role of respirators and surgical masks in mitigating the transmission of SARS-CoV-2 in healthcare settings need to be read with caution, especially when considering the appropriateness of equipment for the purposes of respiratory protection.

These studies have been cited by bodies such as the UK Health Security Agency to provide only limited evidence that N95s were more effective in controlling infection transmission and/or wearer protection. However, few (if any) conclusions can be drawn from them about FFP3 performance within UK healthcare settings.

In determining the question of duties, the matter is clearer. Where there is a risk of exposure of a worker to a significant respiratory hazard which cannot be controlled by other means, including the use of medical devices such as FRSMs, then adequate and suitable RPE must be provided.

Adequate RPE for biological agents is RPE designed to reduce exposure risk to as low as it is reasonably practicable to do so. Thus, if there is a transmission route involving inhalable respiratory particles such as aerosols, even if a contact transmission route is predominant, then that risk has to be reduced by the use of an FFP3 or equivalent.

That is one leg of the legal duty on employers.

However, the RPE also needs to be selected so as to be capable of delivering the designed protection, i.e. that it is suitable. This means that the device fits the intended wearer, and that it can be worn without disturbance in the working conditions the wearer is likely to encounter. That is the second leg of the duty of the employers.

Thus, if an employer provides RPE but it does not fit (the intended wearer(s)) or is not appropriate for the working conditions within which it is used, the employer cannot abandon the use of RPE in favour of another control, such as barrier, if it is known that it would not provide as effective a control as suitable RPE.

In order for RPE to become licensed for use, it needs to meet a range of stringent tests, which consider and address the potential for failure in a range of workplace environments.

If RPE fails to achieve the levels of protection it is designed to achieve in healthcare settings, then this is an indication of the failure of the employer to ensure that RPE has been correctly managed to ensure that it achieves its designed protective capability.

‘If RPE fails to achieve the levels of protection it is designed to achieve in healthcare settings, then this is an indication of the failure of the employer to ensure that RPE has been correctly managed to ensure that it achieves its designed protective capability.

This is undoubtedly a breach of Health and Safety law .’

This is undoubtedly a breach of Health and Safety law. Such a breach must be remedied by finding adequate and suitable alternative RPE with the required Assigned Protection Factor such as powered filtering respirators (as well as instituting other measures from the hierarchy of controls to reduce residual risk). Such other measures may include using barrier (engineering) controls, such as FRSMs. However, FRSMs have never been considered either adequate or suitable equipment for protection against inhalable or respirable risks under COSHH. [ End of document ]

‘ FRSMs have never been considered either adequate or suitable equipment for protection against inhalable or respirable risks under COSHH .’

✾

�� ( Accessed : 20 Oct 2025 ~ British Occupational Hygiene Society / Occupational & Environmental Medicine) COSHH and Healthcare Respiratory Protection: Guidance for Healthcare Employers and Workers on the use of Fluid Resistant Surgical Masks (Type IIR) and respirators (FFP3 etc) to comply with the requirements of the Control of Substances Hazardous to Health Regulations (COSHH) (2002) (England) (Updated 2025) ➤ [ PDF ]

✾

More... On Healthcare Workers

Solutions in... NHS Estates Bulletins

More on... COSHH

From... The UKHSA

“How does Covid being a notifiable disease interact with the UK government discouraging testing?

How does this work? How does it work with NHS Trusts telling their staff not to test?”

Tern, a Priest (28 Aug 2023)

✾

“If we didn’t do any testing, we would have very few cases.”

Donald John Trump (15 May 2020)

✾

More... Healthcare Worker insights

☰ 14 studies & articles on... SARS-CoV-2 (COVID-19) reinfections, cumulative damage, and increased risk of all-cause mortality

Mon, 29 Sep 2025 17:14:14 GMT

‘The arrival of the Omicron variant marked a major shift, introducing numerous extra mutations in the spike gene compared with earlier variants.

Before Omicron, natural infection provided strong and durable protection against reinfection, with minimal waning over time.

However, during the Omicron era, protection was robust only for those recently infected, declining rapidly over time and diminishing within a year.’

‘ Effectiveness of previous infection against reinfection (Omicron) . ’ ➤

�� (5 Feb 2025 ~ Nature) ‘ Differential protection against SARS-CoV-2 reinfection pre- and post-Omicron ’.

❂ Also see:

❦ 9 studies & articles on... SARS-CoV-2 (COVID-19) vaccines, ‘Omicron’, and waning protection ➲

❦ The ‘ Omicron ’ Era (late 2021–).

➲ Data accessed: 7 September 2025 .

➲ Genomic epidemiology of SARS-CoV-2 since pandemic start, by date .

❦ On SARS-CoV-2 reinfections, and their cumulative danger

�� (5 Feb 2025 ~ Nature) Differential protection against SARS-CoV-2 reinfection pre- and post-Omicron ➤

‘The arrival of the Omicron variant marked a major shift , introducing numerous extra mutations in the spike gene compared with earlier variants.

Before Omicron , natural infection provided strong and durable protection against reinfection , with minimal waning over time.

However, during the Omicron era , protection was robust only for those recently infected , declining rapidly over time and diminishing within a year .’

�� (10 Oct 2024 ~ The Lancet: Regional Health ~ Western Pacific) Long COVID facts and findings: a large-scale online survey in 74,075 Chinese participants ➤

‘ While acute symptoms of reinfection are generally milder , the severity and incidence rate of long COVID [ PASC ] increase significantly with the number of reinfections . ’

“ Anything that is more transmissible will kill in two ways.

Infecting more people.

Worsening pressure on healthcare. ”

Dr. Noor Bari, Emergency Medicine (2023) ➲

�� (20 Mar 2025 ~ Canadian Broadcasting Corporation) Beyond long COVID – how reinfections could be causing silent long-term organ damage ➲

“There was a recent 2024 study showing us that individuals who survive an acute COVID-19 infection – these are not individuals who are getting diagnosed with long COVID – on average will lose somewhere in the neighbourhood of two to six IQ points per infection .”

�� (7 Jan 2025 ~ The Lancet: Regional Health ~ Americas) SARS-COV-2 re-infection and incidence of post-acute sequelae of COVID-19 (PASC) among essential workers in New York: a retrospective cohort study ➤

‘After adjusting for relevant demographic, lifestyle, and clinical variables, we found a significant association between the risk of experiencing PASC [ P ost- A cute S equelae of C OVID-19 , or ‘Long Covid’ ] and multiple SARS-COV-2 infections , severe COVID-19, and being unvaccinated at first infection.’

�� (27 Mar 2024 ~ BMC Infectious Diseases) The symptoms and interval of Omicron SARS-CoV-2 reinfection among healthcare workers in a hospital of Southern China: a cross-sectional study ➤

‘The main symptoms during the first infection in this Omicron wave were fever and sore throat, while sore throat was the main symptom in the reinfection; the average interval for SARS-CoV-2 [COVID-19] reinfection was 149.91 days .

The reasons for COVID-19 reinfection are multifaceted , primarily including low antibody levels , the shortened duration of immune protection provided by antibodies, the mutation of viral strains , non-adherence to epidemic prevention measures by the population, hesitancy towards vaccination , and public fatigue due to the prolonged pandemic.’

�� (29 Feb 2024 ~ CIDRAP) Even fully recovered survivors of mild COVID can lose IQ points, study suggests ➤

‘COVID-19 vaccination provided a small cognitive benefit , while reinfection was tied to an IQ loss of nearly 2 points , compared with no reinfection.’

�� (22 Feb 2024 ~ Science) Solving the puzzle of Long Covid ➲

‘ Reinfection , which is now the dominant type of SARS-CoV-2 infection , is not inconsequential; it can trigger de novo Long Covid [ PASC ] or exacerbate its severity .

Each reinfection contributes additional risk of Long Covid: cumulatively , two infections yield a higher risk of Long Covid than one infection, and three infections yield a higher risk than two infections.’

�� (17 Feb 2024 ~ The Lancet: eClinical Medicine) Long-term risks of respiratory diseases in patients infected with SARS-CoV-2: a longitudinal, population-based cohort study ➲

‘ Our study showed a significant increase of the long-term risk of developing asthma, COPD [chronic obstructive pulmonary disease] , ILD [interstitial lung disease] , and lung cancer diseases among individuals who suffered SARS-CoV-2 reinfection . ’

�� (7 Feb 2024 ~ Journal of Microbiology, Immunology and Infection) Risk factors and mortality of SARS-CoV-2 reinfection during the Omicron era in Taiwan: A nationwide population-based cohort study ➤

‘ During the SARS-CoV-2 Omicron era, reinfection patients were observed to have an increased risk of all-cause mortality . ’

�� (2 Feb 2024 ~ Nature: Communications) Risk of SARS-CoV-2 reinfection during multiple Omicron variant waves in the UK general population ➤

‘ The estimated risk of confirmed reinfection in the Omicron waves is high , and is associated with both viral evolution and waning immunity , but confirmed reinfections have lower viral loads and fewer symptoms than the first identified infections.

Additional protection from vaccination also decreases over time .

Given the waning immunity from previous infection and vaccination , and the stronger immune evasion from most recent Omicron variants , reinfection risk remains high , and on-going evaluation of hybrid immunity against emerging dominant variants remains important to pandemic control and vaccination policy .

Further public health measures may be needed to help protect vulnerable people from reinfection . ’

�� (8 Dec 2023 ~ Statistics Canada / Statistique Canada) Experiences of Canadians with long-term symptoms following COVID-19 ➤

‘ As of June 2023 , about 2 in 3 Canadians reported at least one infection , with 1 in 5 having been infected multiple times . ’

�� (14 Apr 2023 ~ Viruses) SARS-CoV-2 Reinfection and Severity of the Disease: A Systematic Review and Meta-Analysis ➤

‘ Reinfections were more prevalent during the Omicron variant period . The mean age of reinfected patients was 38 years , and females were predominant among reinfected patients.

Reinfection with SARS-CoV-2 suggests that natural immunity is not long-lasting in COVID-19 patients. ’

�� (10 Nov 2022 ~ Nature: Medicine) Acute and post-acute sequelae associated with SARS-CoV-2 reinfection ➤

‘ Reinfection further increases risks of death , hospitalization and sequelae in multiple organ systems in the acute [short-term] and post-acute phase . ’

�� (25 May 2022 ~ Nature: Medicine) Long COVID after breakthrough SARS-CoV-2 infection ➤

‘ At 6 months after infection, beyond the first 30 days of illness, compared to contemporary controls, people with breakthrough SARS-CoV-2 infection (‘BTI’, or reinfection ) exhibited a higher risk of death and incident post-acute sequelae , including cardiovascular , coagulation and hematologic , gastrointestinal , kidney , mental health , metabolic , musculoskeletal and neurologic disorders . ’

✾

“ If you are letting yourself get infected and taking no precautions against passing it on, you are not a passive bystander for your next infection.

You’ve participated in creating it. ”

Dr. Noor Bari, Emergency Medicine (2024) ➲

✾

❦ SARS-CoV-2 (COVID-19) variants of concern (VOC), and ‘Omicron’ .

➲ Data accessed: 29 October 2024 .

➲ Genomic epidemiology of SARS-CoV-2 since pandemic start . ➲

❦ SARS-CoV-2 (COVID-19) variants of concern (VOC), and ‘Omicron’ .

➲ Data accessed: 29 September 2025 .

➲ Genomic epidemiology of SARS-CoV-2 since pandemic start . ➲

More ... On reinfections

More ... On variants, immunity, and vaccines

More by ... Dr. Noor Bari

☰ 9 studies & articles on... SARS-CoV-2 (COVID-19) vaccines, ‘Omicron’, and waning protection

Sun, 07 Sep 2025 12:06:15 GMT

‘Vaccine effectiveness against SARS-CoV-2 [COVID-19] infection declines markedly with time and Omicron variants.’

from ‘Effectiveness of COVID-19 vaccines against SARS-CoV-2 infection and severe outcomes in adults’ by Zhou et al / European Respiratory Review (2024).

❦ The ‘ Omicron ’ Era (late 2021–).

➲ Data accessed: 7 September 2025 .

➲ Genomic epidemiology of SARS-CoV-2 since pandemic start, by date .

❦ On waning vaccines, and the ‘Omicron’ variant (late 2021–)

�� (5 Feb 2025 ~ Nature) Differential protection against SARS-CoV-2 reinfection pre- and post-Omicron ➤

‘ The arrival of the Omicron variant [ in late 2021 ] marked a major shift , introducing numerous extra mutations in the spike gene compared with earlier variants.

These evolutionary changes have raised concerns regarding their potential impact on immune evasion , disease severity and the effectiveness of vaccines and treatments . ’

�� (19 Feb 2025 ~ European Respiratory Review) Effectiveness of COVID-19 vaccines against SARS-CoV-2 infection and severe outcomes in adults: a systematic review and meta-analysis of European studies published up to 22 January 2024 ➤

‘ Vaccine effectiveness against SARS-CoV-2 [ COVID-19 ] infection declines markedly with time and Omicron variants . ’

�� (9 Apr 2025 ~ Pharma Times) NHS launches spring COVID-19 booster campaign ➤

‘ Eligible [ UK ] groups are being offered an additional [ ‘COVID-19 vaccine booster’ ] to increase protection against the virus. These include everyone aged 75 years and over , residents of older adult care homes, and people aged six months and over with weakened immune systems .

Alex Allen, consultant epidemiologist at the UK Health Security Agency [ UKHSA ] , said last year’s spring programme proved effective.

“It reduced the risk of getting severely ill and being hospitalised by over 40% in those at greatest risk – for up to nine weeks after vaccination.” ’

“ Anything that is more transmissible will kill in two ways.

Infecting more people.

Worsening pressure on healthcare. ”

Dr. Noor Bari, Emergency Medicine (2023) ➲

�� (27 Feb 2025 ~ CDC) Interim Estimates of 2024–2025 COVID-19 Vaccine Effectiveness Among Adults Aged ≥18 Years — VISION and IVY Networks, September 2024–January 2025 ➤

‘ Vaccine effectiveness (VE) of 2024–2025 COVID-19 vaccine was 33% against COVID-19–associated emergency department or urgent care visits among adults aged ≥18 years , and 45%–46% against hospitalizations among immunocompetent adults aged ≥65 years , compared with not receiving a 2024–2025 vaccine dose.

VE against hospitalizations in immunocompromised adults aged ≥65 years was 40% . ’

❦ SARS-CoV-2 (COVID-19) variants of concern (VOC), and ‘Omicron’ .

➲ Data accessed: 29 October 2024 .

➲ Genomic epidemiology of SARS-CoV-2 since pandemic start . ➲

�� (6 Aug 2024 ~ Clinical Infectious Diseases) Effectiveness of Updated 2023–2024 (Monovalent XBB.1.5) COVID-19 Vaccination Against SARS-CoV-2 Omicron XBB and BA.2.86/JN.1 Lineage Hospitalization and a Comparison of Clinical Severity—IVY Network, 26 Hospitals, 18 October 2023–9 March 2024 ➤

‘ Omicron BA.2.86 and its descendants, including JN.1 (referred to as ‘JN lineages’), emerged in late 2023 and exhibited substantial divergence from co-circulating [ Omicron ] XBB lineages.

Vaccine effectiveness in the first 7–89 days after receipt of an updated [ 2023–2024 monovalent XBB.1.5 vaccine ] dose was 54.2% against XBB lineage hospitalization , and 32.7% against JN lineage hospitalization . ’

�� (1 Aug 2024 ~ JAMA Internal Medicine) Estimated Effectiveness of the BNT162b2 XBB Vaccine Against COVID-19 ➤

‘ Effectiveness... of the [ Pfizer ] BNT162b2 XBB vaccine was 62% against COVID-19 hospitalization , and 58% for Emergency Department or Urgent Care visits .

Older versions of COVID-19 vaccines offered little , if any , long-term protection , including against hospital admission , regardless of the number or type of prior doses received. ’

Nb. Conflict of Interest Disclosures :

Dr Tartof reported institutional grants from Pfizer and GSK outside the submitted work. Dr Slezak reported institutional grants from Pfizer and Dynavax outside the submitted work. Mr Frankland reported a research contract with Pfizer and previous stock in Pfizer . Dr Puzniak reported personal fees from Pfizer during the conduct of the study . Ms Hong reported institutional grants from Pfizer during the conduct of the study . Dr Ackerson reported institutional grants from Pfizer , Moderna , GSK , and Dynavax outside the submitted work. Dr Stern reported grants from GSK , Sanofi , and Moderna outside the submitted work. Dr Jodar reported salary from and stock in Pfizer outside the submitted work. Dr McLaughlin reported salary from and stock in Pfizer during the conduct of the study . No other disclosures were reported.

“No other disclosures were reported.”

Well, thank goodness for that.

Maybe that’s why they had to end the piece with ‘...the BNT162b2 XBB vaccine provided statistically significant additional protection against a range of COVID-19 outcomes.’

Like what – having an itchy earlobe?

If 60:40 is significant protection against an A&E visit or hospital admission , I’d hate to see the odds for insignificant protection.

�� (29 May 2024 ~ The New England Journal of Medicine) Durability of XBB.1.5 Vaccines against Omicron Subvariants ➤

‘ The [ Omicron XBB.1.5 ] vaccine effectiveness against infection reached a level of 52.2% after 4 weeks . It decreased to 32.6% after 10 weeks and to 20.4% after 20 weeks .

The effectiveness against hospitalization reached a level of 66.8% after 4 weeks , and decreased to 57.1% after 10 weeks .

The [ Omicron ] XBB.1.5 vaccines were less protective against [ Omicron ] JN.1 than against XBB sublineages. ’

�� (2 Feb 2024 ~ Nature: Communications) Risk of SARS-CoV-2 reinfection during multiple Omicron variant waves in the UK general population ➤

‘The estimated risk of confirmed reinfection in the Omicron waves is high , and is associated with both viral evolution and waning immunity , but confirmed reinfections have lower viral loads and fewer symptoms than the first identified infections.

Additional protection from vaccination also decreases over time .

Given the waning immunity from previous infection and vaccination , and the stronger immune evasion from most recent Omicron variants , reinfection risk remains high , and on-going evaluation of hybrid immunity against emerging dominant variants remains important to pandemic control and vaccination policy .

Further public health measures may be needed to help protect vulnerable people from reinfection .’

�� (25 May 2022 ~ Nature: Medicine) Long COVID after breakthrough SARS-CoV-2 infection ➤

‘ Vaccination before infection confers only partial protection in the post-acute phase of the disease. ’

✾

More ... On variants, immunity and vaccines

More ... On reinfections

❦ More C-19 Cartoons ➲

☰ For Medics ~ 16 studies & articles on... SARS-CoV-2 (COVID-19) and on-going mitochondrial dysfunction

Fri, 29 Aug 2025 14:50:02 GMT

‘... SARS-CoV-2 infection causes prolonged disruptions in mitochondrial function, significantly altering cellular energy metabolism.’

‘ A schematic diagram showing the significant contribution of SCoV2-induced altered mitochondrial dynamics and mitochondrial EGFR translocation in sustaining viral propagation.

First, SCoV2 RNA and nucleocapsid complex increase ΔΨm during the early stages of SCoV2 infection. This alteration subsequently promotes mitochondrial elongation. SCoV2 also activates the mitochondrial OXPHOS process, thereby promoting ATP production.

Second, SCoV2 activates EGFR-mediated cell survival signalling and subsequently promotes mitochondrial EGFR internalisation, which contributes to the maintenance of abnormal mitochondrial bioenergetics.

These alterations are physiologically relevant to the maintenance of homoeostasis of SCoV2-infected cells and robust SCoV2 propagation. ’

�� (11 May 2024 ~ Nature: Signal Transduction and Targeted Therapy) SARS-CoV-2 aberrantly elevates mitochondrial bioenergetics to induce robust virus propagation ➤

❦ On mitochondria and dysfunction

❦ What are mitochondria?

Mitochondria are small organelles found in nearly all human cells , and are vital to survival .

They are often referred to as the “ powerhouses of the cell ” because they generate most of the energy needed for cellular functions by producing adenosine triphosphate ( ATP ).

Mitochondria also play roles in cell-signalling , cell growth , and cell death ( apoptosis ).

❦ Mitochondrial dysfunction and disease

When mitochondria stop functioning , the cell they are in is starved of energy . Depending on the type of cell, symptoms can vary widely.

As a general rule , cells that need the largest amounts of energy – such as heart muscle cells and nerves – are affected the most by faulty mitochondria.

Although symptoms of a mitochondrial disease vary greatly , they might include :

loss of muscle co-ordination and weakness
problems with vision or hearing
heart , liver , or kidney disease
gastrointestinal problems
neurological problems , including dementia .

❦ Notes

What are mitochondria? (Medical News Today) ➤
Types of Mitochondrial Disease (United Mitochondrial Disease Foundation) ➤

�� (12 Aug 2025 ~ Annals of Medicine) Mitochondrial function is impaired in long COVID patients ➤

‘ Fatigue, reduced exercise tolerance and hyperlactataemia on minimal exertion [in ‘Long COVID’/ PASC cases] have led to the suggestion of a bioenergetic defect.

In conclusion, this study identifies mitochondrial function abnormalities in the PBMCs of Long COVID/PASC cases which are distinct from the mitochondrial phenotype of acute SARS-CoV-2 infection.

Our findings are consistent with the hypothesis that there is an abnormality of complex V function which is evidence of bioenergetic inefficiency.

The results suggest that PBMC mitochondrial function might be a future biomarker of Long COVID/PASC. ’

�� (30 Jul 2025 ~ Mitochondrion) Peripheral immune progression to long COVID is associated with mitochondrial gene transcription: A meta-analysis ➤

‘ We conducted one of the most comprehensive meta-analyses to date of all quality bulk RNA-seq studies worldwide from the COVID-19 pandemic and show significant mitochondrial transcript changes in the peripheral immune system of people with Long COVID, with unexpectedly low levels of intracellular viral RNA in Long COVID.

This extensive analysis, which includes 26 studies and 1,272 individuals, shows that mononuclear cells, PBMC, and granulocytes from Long COVID patients exhibit significant alterations in mitochondrial genes and related processes. ’

�� (12 Jul 2025 ~ Molecular Psychiatry) Brain and muscle chemistry in myalgic encephalitis/chronic fatigue syndrome (ME/CFS) and long COVID: a 7T magnetic resonance spectroscopy study ➤

‘ An observation of potential importance for future research and treatment development is that the ME/CFS and long COVID groups tested in this study differed in terms of their brain neurochemistry measured by MRS.

It is therefore possible that the underlying neurobiological mechanisms, while leading to similar clinical presentation of fatigue and brain fog, may differ between these groups.

While this needs to be verified with future research, an important implication is that patients with ME/CFS and those with fatigue in the course of long COVID should not be studied as a single group, at least until the mechanisms are better understood. ’

�� (8 Jul 2025 ~ PNAS) Oxidative stress is a shared characteristic of ME/CFS and Long COVID ➤

‘ More than 65 million individuals worldwide are estimated to have Long COVID (LC), wherein individuals after infection report persistent fatigue, post-exertional malaise (PEM) , and other symptoms resembling myalgic encephalomyelitis /chronic fatigue syndrome (ME/CFS).

With no clinically approved treatments or diagnostic markers for these conditions, there is an urgent need to define the molecular underpinnings.

By studying bioenergetic characteristics of immune cells in healthy controls, ME/CFS, and LC donors, we find lymphocytes from ME/CFS and LC donors exhibit elevated oxidative stress.

Due to excess oxidative stress and consequent mitochondrial damage, ME/CFS and LC donor lymphocytes consume excess host energy, contributing to debilitating fatigue and other sequelae. ’

�� (9 May 2025 ~ International Journal of Molecular Sciences) Persistent Monocytic Bioenergetic Impairment and Mitochondrial DNA Damage in PASC Patients with Cardiovascular Complications ➤

‘ This study identifies persistent mitochondrial dysfunction in long COVID monocytes as a critical driver of cardiovascular complications in PASC.

Key defects – bioenergetic failure, impaired stress adaptation and mtDNA damage – correlate with clinical symptoms like heart failure and exercise intolerance. ’

�� (4 Nov 2024 ~ GeroScience) Novel biomarkers of mitochondrial dysfunction in Long COVID patients ➤

‘ COVID-19 can lead to severe acute respiratory syndrome, and while most individuals recover within weeks, approximately 30–40% experience persistent symptoms collectively known as Long COVID, post-COVID-19 syndrome, or post-acute sequelae of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection (PASC).

According to recent studies, SARS-CoV-2 infection causes prolonged disruptions in mitochondrial function, significantly altering cellular energy metabolism.

Our research employed transmission electron microscopy to reveal distinct mitochondrial structural abnormalities in Long COVID patients, notably including significant swelling, disrupted cristae, and an overall irregular morphology, which collectively indicates severe mitochondrial distress. ’

�� (30 Apr 2024 ~ Pharmacological Research) SARS-CoV-2 mitochondrial metabolic and epigenomic reprogramming in COVID-19 ➤

‘ To determine the effects of SARS-CoV-2 infection on cellular metabolism, we conducted an exhaustive survey of the cellular metabolic pathways modulated by SARS-CoV-2 infection and confirmed their importance for SARS-CoV-2 propagation by cataloging the effects of specific pathway inhibitors.

This revealed that SARS-CoV-2 strongly inhibits mitochondrial oxidative phosphorylation (OXPHOS) resulting in increased mitochondrial reactive oxygen species (mROS) production.

The elevated mROS stabilizes HIF-1α which redirects carbon molecules from mitochondrial oxidation through glycolysis and the pentose phosphate pathway (PPP) to provide substrates for viral biogenesis. mROS also induces the release of mitochondrial DNA (mtDNA) which activates innate immunity.

The restructuring of cellular energy metabolism is mediated in part by SARS-CoV-2 Orf8 and Orf10 whose expression restructures nuclear DNA (nDNA) and mtDNA OXPHOS gene expression.

These viral proteins likely alter the epigenome, either by directly altering histone modifications or by modulating mitochondrial metabolite substrates of epigenome modification enzymes, potentially silencing OXPHOS gene expression and contributing to long-COVID. ’

�� (25 Aug 2023 ~ Frontiers in Cellular Infectious Microbiology) Host mitochondria: more than an organelle in SARS-CoV-2 infection ➤

‘ The severe form of COVID-19 is often marked by an altered immune response and cytokine storm. Advanced age, age-related and underlying diseases, including metabolic syndromes, appear to contribute to increased COVID-19 severity and mortality suggesting a role for mitochondria in disease pathogenesis.

Furthermore, since the immune system is associated with mitochondria and its damage-related molecular patterns (mtDAMPs), the host mitochondrial system may play an important role during viral infections.

Viruses have evolved to modulate the immune system and mitochondrial function for survival and proliferation, which in turn could lead to cellular stress and contribute to disease progression.

Recent studies have focused on the possible roles of mitochondria in SARS-CoV-2 infection. It has been suggested that mitochondrial hijacking by SARS-CoV-2 could be a key factor in COVID-19 pathogenesis.

In this review, we discuss the roles of mitochondria in viral infections, including SARS-CoV-2 infection, based on past and present knowledge. ’

�� (9 Aug 2023 ~ Science Translational Medicine) Core mitochondrial genes are down-regulated during SARS-CoV-2 infection of rodent and human hosts ➤

‘ SARS-CoV-2 needs host cells to generate molecules for viral replication and propagation.

Guarnieri et al now show that the virus is able to block expression of both nuclear-encoded and mitochondrial-encoded mitochondrial genes, resulting in impaired host mitochondrial function.

They analyzed human nasopharyngeal samples and autopsy tissues from patients with COVID-19 and tissues from hamsters and mice infected with SARS-CoV-2.

Host cells attempt to compensate by activating innate immune defenses and mitochondrial gene expression, but chronically impaired mitochondrial function ultimately may result in serious COVID-19 sequelae such as organ failure. ’

�� (21 Jan 2022 ~ iScience) SARS-CoV-2 infection enhances mitochondrial PTP complex activity to perturb cardiac energetics ➤

‘ Here, we conducted transcriptomic analysis of human PBMCs, identified significant changes in mitochondrial, ion channel, and protein quality-control gene products.

SARS-CoV-2 proteins selectively target cellular organelle compartments, including the endoplasmic reticulum and mitochondria.

M-protein, NSP6, ORF3A, ORF9C, and ORF10 bind to mitochondrial PTP complex components cyclophilin D, SPG-7, ANT, ATP synthase, and a previously undescribed CCDC58 (coiled-coil domain containing protein 58).

Knockdown of CCDC58 or mPTP blocker cyclosporin A pretreatment enhances mitochondrial Ca2+ retention capacity and bioenergetics.

SARS-CoV-2 infection exacerbates cardiomyocyte autophagy and promotes cell death that was suppressed by cyclosporin A treatment.

Our findings reveal that SARS-CoV-2 viral proteins suppress cardiomyocyte mitochondrial function that disrupts cardiomyocyte Ca2+ cycling and cell viability. ’

�� (17 Dec 2021 ~ iScience) Immune system cells from COVID-19 patients display compromised mitochondrial-nuclear expression co-regulation and rewiring toward glycolysis ➤

‘ Here, we analyzed available bulk RNA-seq datasets from COVID-19 patients and corresponding healthy controls (three blood datasets, N = 48 healthy, 119 patients; two respiratory tract datasets, N = 157 healthy, 524 patients).

We found significantly reduced mtDNA gene expression in blood, but not in respiratory tract samples from patients.

Next, analysis of eight single-cells RNA-seq datasets from peripheral blood mononuclear cells, nasopharyngeal samples, and Bronchoalveolar lavage fluid (N = 1,192,243 cells), revealed significantly reduced mtDNA gene expression especially in immune system cells from patients.

This is associated with elevated expression of nuclear DNA-encoded OXPHOS subunits, suggesting compromised mitochondrial-nuclear co-regulation.

This, together with elevated expression of ROS-response genes and glycolysis enzymes in patients, suggest rewiring toward glycolysis, thus generating beneficial conditions for SARS-CoV-2 replication.

Our findings underline the centrality of mitochondrial dysfunction in COVID-19. ’

�� (15 Mar 2021 ~ Nature Communications) SARS-CoV-2 hijacks folate and one-carbon metabolism for viral replication ➤

‘ The recently identified Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is the cause of the COVID-19 pandemic.

How this novel beta-coronavirus virus, and coronaviruses more generally, alter cellular metabolism to support massive production of ~30 kB viral genomes and subgenomic viral RNAs remains largely unknown.

To gain insights, transcriptional and metabolomic analyses are performed 8 hours after SARS-CoV-2 infection, an early timepoint where the viral lifecycle is completed but prior to overt effects on host cell growth or survival.

Here, we show that SARS-CoV-2 remodels host folate and one-carbon metabolism at the post-transcriptional level to support de novo purine synthesis, bypassing viral shutoff of host translation.

Intracellular glucose and folate are depleted in SARS-CoV-2-infected cells, and viral replication is exquisitely sensitive to inhibitors of folate and one-carbon metabolism, notably methotrexate.

Host metabolism targeted therapy could add to the armamentarium against future coronavirus outbreaks. ’

�� (6 Jan 2021 ~ American Journal of Physiology Cell Physiology) Mitochondrial metabolic manipulation by SARS-CoV-2 in peripheral blood mononuclear cells of patients with COVID-19 ➤

‘ Patients with metabolic syndrome suffer from severe complications and a higher mortality rate due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection.

We recently proposed that SARS-CoV-2 can hijack host mitochondrial function and manipulate metabolic pathways for their own advantage.

The aim of the current study was to investigate functional mitochondrial changes in live peripheral blood mononuclear cells (PBMCs) from patients with COVID-19 and to decipher the pathways of substrate utilization in these cells and corresponding changes in the inflammatory pathways.

We demonstrate mitochondrial dysfunction, metabolic alterations with an increase in glycolysis, and high levels of mitokine in PBMCs from patients with COVID-19.

Interestingly, we found that levels of fibroblast growth factor 21 mitokine correlate with COVID-19 disease severity and mortality.

These data suggest that patients with COVID-19 have a compromised mitochondrial function and an energy deficit that is compensated by a metabolic switch to glycolysis.

This metabolic manipulation by SARS-CoV-2 triggers an enhanced inflammatory response that contributes to the severity of symptoms in COVID-19. Targeting mitochondrial metabolic pathway(s) can help define novel strategies for COVID-19. ’

�� (20 Jul 2020 ~ American Journal of Physiology Cell Physiology) Decoding SARS-CoV-2 hijacking of host mitochondria in COVID-19 pathogenesis ➤

‘ Based on available data for the SARS-CoV-1 virus, we suggest how CoV-2 localization of RNA transcripts in mitochondria hijacks the host cell’s mitochondrial function to viral advantage.

Besides viral RNA transcripts, RNA also localizes to mitochondria.

SARS-CoV-2 may manipulate mitochondrial function indirectly, first by ACE2 regulation of mitochondrial function, and once it enters the host cell, open-reading frames (ORFs) such as ORF-9b can directly manipulate mitochondrial function to evade host cell immunity and facilitate virus replication and COVID-19 disease.

Manipulations of host mitochondria by viral ORFs can release mitochondrial DNA (mtDNA) in the cytoplasm and activate mtDNA-induced inflammasome and suppress innate and adaptive immunity.

We argue that a decline in ACE2 function in aged individuals, coupled with the age-associated decline in mitochondrial functions resulting in chronic metabolic disorders like diabetes or cancer, may make the host more vulnerable to infection and health complications to mortality.

These observations suggest that distinct localization of viral RNA and proteins in mitochondria must play essential roles in SARS-CoV-2 pathogenesis.

Understanding the mechanisms underlying virus communication with host mitochondria may provide critical insights into COVID-19 pathologies. An investigation into the SARS-CoV-2 hijacking of mitochondria should lead to novel approaches to prevent and treat COVID-19. ’

�� (17 Jul 2020 ~ Cell Metabolism) Elevated glucose levels favor SARS-CoV-2 infection and monocyte response through a HIF-1alpha/Glycolysis-Dependent Axis ➤

‘ COVID-19 can result in severe lung injury.

It remained to be determined why diabetic individuals with uncontrolled glucose levels are more prone to develop the severe form of COVID-19.

The molecular mechanism underlying SARS-CoV-2 infection and what determines the onset of the cytokine storm found in severe COVID-19 patients are unknown.

Monocytes and macrophages are the most enriched immune cell types in the lungs of COVID-19 patients and appear to have a central role in the pathogenicity of the disease.

These cells adapt their metabolism upon infection and become highly glycolytic, which facilitates SARS-CoV-2 replication.

The infection triggers mitochondrial ROS production, which induces stabilization of hypoxia-inducible factor-1α (HIF-1α) and consequently promotes glycolysis.

HIF-1α-induced changes in monocyte metabolism by SARS-CoV-2 infection directly inhibit T cell response and reduce epithelial cell survival.

Targeting HIF-1ɑ may have great therapeutic potential for the development of novel drugs to treat COVID-19. ’

‘ Dear Secretary Robert Kennedy Jr * , with your expressed concern about many children now showing signs of mitochondrial dysfunction, here is evidence that a pathogen we continue to allow to circulate without mitigations is known to cause mitochondrial dysfunction. ’

by Dr. Andrew Urquhart, 29 Aug 2025 (Twitter / X ➤ )

* United States of America’s Secretary of Health and Human Services (HHS) (Feb 13, 2025 –)

❦ Studies presented on this page collated by Dr. Andrew Urquhart (PhD) . Excerpts collated by C19.Life.

More ... ☰ Lists

More by ... C19.Life

☣ Variant Watch: 📖 Antigenic and virological characteristics of SARS-CoV-2 variants BA.3.2, XFG, and NB.1.8.1

Thu, 05 Jun 2025 17:32:17 GMT

‘Importantly, NB.1.8.1 shows a balanced profile of ACE2 binding and immune evasion, supporting its potential for future prevalence.’

(Accessed 29 Sep 2025 ) Genomic epidemiology of SARS-CoV-2 with subsampling focused globally since pandemic start, showing emergence and progression of XFG , NB.1.8.1 and BA.3.2 . ➲

❦ Correspondence ~ ‘ Antigenic and virological characteristics of SARS-CoV-2 variants BA.3.2, XFG, and NB.1.8.1 ’

By Guo et al / The Lancet: Infectious Diseases ( 5 Jun 2025 )

‘The SARS-CoV-2 saltation variant BA.3.2, harbouring over 50 mutations relative to its ancestral BA.3 lineage, has recently drawn global attention.

Notably, BA.3.2 exhibits 44 mutations distinct from the currently dominant LP.8.1/LP.8.1.1 variant, raising speculation about its potential to drive an outbreak similar to BA.2.86/JN.1, particularly following its first detection outside South Africa in the Netherlands on April 2, 2025 .

Concurrently, multiple emerging variants – including NB.1.8.1 , LF.7.9 , XEC.25.1 , XFH , and XFG – exhibit enhanced growth advantages over LP.8.1.1 , which suggests their potential to dominate future transmission waves.

These variants show convergent evolution .

In summary, our findings indicate that BA.3.2 exhibits robust antibody evasion but has low ACE2-binding capability and infectivity , which substantially limits its likelihood of prevailing.

To achieve efficient spread akin to BA.2.86 or JN.1, BA.3.2 would require additional mutations to improve both its receptor engagement efficiency and its evasion of class 1 antibodies.

Similarly, although XFG displays strong immune evasion , its relatively low ACE2 engagement efficiency suggests that it might need compensatory mutations to enhance receptor compatibility for sustained transmission.

Importantly, NB.1.8.1 shows a balanced profile of ACE2 binding and immune evasion , supporting its potential for future prevalence . ’

�� ( 5 Jun 2025 ~ The Lancet: Infectious Diseases ) Antigenic and virological characteristics of SARS-CoV-2 variants BA.3.2, XFG, and NB.1.8.1 ➤

�� (5 Jun 2025 ~ The Lancet: Infectious Diseases) ‘ Antigenic and virological characteristics of SARS-CoV-2 variants BA.3.2, XFG, and NB.1.8.1. ’

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More... Variants

☣ Variant Watch: 📖 Host cell entry and neutralisation sensitivity of SARS-CoV-2 BA.3.2

Tue, 03 Jun 2025 15:16:01 GMT

‘Since late 2024, a potential third major evolutionary shift in SARS-CoV-2 evolution might be unfolding.

In November 2024 and January 2025, a highly mutated descendant of the Omicron subvariant BA.3 was detected in South Africa.’

(Accessed 29 Sep 2025 ) Genomic epidemiology of SARS-CoV-2 with subsampling focused globally since pandemic start, showing emergence of BA.3.2 . ➲

❦ Correspondence ~ ‘ Host cell entry and neutralisation sensitivity of SARS-CoV-2 BA.3.2 ’

By Zhang et al / The Lancet: Microbe ( 3 Jun 2025 )

‘The COVID-19 pandemic and the ensuing endemic have been characterised by the continuous emergence of novel SARS-CoV-2 variants , each showing augmented antibody evasion due to mutations in the viral spike (S) protein.

These new variants usually harbour a few S protein mutations, conferring a modest growth advantage within the population.

‘However, a quantum leap of SARS-CoV-2 evolution was observed on two occasions .

The first occurred at the end of 2021 , when the highly mutated Omicron variant (B.1.1.529) became dominant, showing unprecedented antibody evasion .’ *

* �� (3 Feb 2022 ~ Cell) The Omicron variant is highly resistant against antibody-mediated neutralization: Implications for control of the COVID-19 pandemic ➤

‘The second major evolutionary shift was observed in July 2023 , when the subvariant BA.2.86 – a highly mutated descendant of the BA.2 variant – emerged and dominated globally in 2024 .’ *

* �� (27 Sep 2023 ~ The Lancet: Infectious Diseases) Sensitivity of the SARS-CoV-2BA.2.86 variant to prevailing neutralising antibody responses ➤

�� (18 Sep 2023 ~ The Lancet: Infectious Diseases) Transmissibility, infectivity, and immune evasion of the SARS-CoV-2 BA.2.86 variant ➤

�� (19 Sep 2023 ~ The Lancet: Infectious Diseases) Antigenicity and infectivity characterisation of SARS-CoV-2 BA.2.86 ➤

�� (1 Feb 2024 ~ Cell) SARS-CoV-2 BA.2.86 enters lung cells and evades neutralizing antibodies with high efficiency ➤

Since late 2024 , a potential third major evolutionary shift in SARS-CoV-2 evolution might be unfolding. In November 2024 and January 2025, a highly mutated descendant of the Omicron subvariant BA.3 was detected in South Africa *.

* �� (18 May 2022 ~ The New England Journal of Medicine) Neutralization of the SARS-CoV-2 Deltacron and BA.3 Variants ➤

In April 2025 , the variant, designated as BA.3.2 , was also detected in the Netherlands, raising the possibility of global dissemination. BA.3.2 harbours more than 50 S protein mutations compared with BA.3, which might have profoundly altered the cell entry and antibody-mediated neutralisation of BA.3.2.

Our findings suggest that BA.3.2 (A) and BA.3.2 (B) might enter cells slightly less efficiently than the parental BA.3 variant; however, BA.3.2 (A) and BA.3.2 (B) might be able to evade the neutralising antibodies used for COVID-19 therapy or those induced by vaccination with a markedly higher efficiency .

The evasion of antibodies by the variants in individuals vaccinated with the JN.1-booster vaccine was similar to , or greater than , that observed for the currently dominating LP.8.1.1 variant . [ Note: this is not a good thing. ]

These observations suggest that BA.3.2 – particularly BA.3.2 (B) – may disseminate within populations with high antibody levels, thereby warranting close monitoring. ’

�� ( 3 Jun 2025 ~ The Lancet: Microbe ) Host cell entry and neutralisation sensitivity of SARS-CoV-2 BA.3.2 ➤

�� (3 Jun 2025 ~ The Lancet: Microbe) ‘ Host cell entry and neutralisation sensitivity of SARS-CoV-2 BA.3.2 .’

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More... Variants

❦ Some thoughts and essays by Dr. Lisa Iannattone

Sat, 19 Apr 2025 20:15:41 GMT

“There’s nothing radical about clean air and compassion.”

Thoughts and essays by Dr. Lisa Iannattone.

❂

Thoughts & essays by... Dr. Noor Bari

❦ Some thoughts and essays by Dr. Noor Bari

Fri, 18 Apr 2025 19:22:23 GMT

“We are drunk-driving in healthcare... with a pathogen that has a 10% fatality rate in that setting.”

Thoughts and essays by Dr. Noor Bari.

❂

Some thoughts & essays by... Dr. Lisa Iannattone

📖 COVID-19 may put patients at risk for other infections for at least 1 year

Wed, 02 Apr 2025 13:26:17 GMT

‘These findings have important implications for understanding the potential impact of COVID-19 on long-term immune function and susceptibility to pathogens.’

�� (2 Apr 2025 ~ CIDRAP) ‘ COVID-19 may put patients at risk for other infections for at least 1 year ’.

❦ Scientific Media Article ~ ‘ COVID-19 may put patients at risk for other infections for at least 1 year ’

By Stephanie Soucheray / CIDRAP ( 2 Apr 2025 )

‘In a study yesterday in The Lancet Infectious Diseases , its authors describe how a positive test for COVID-19 is associated with increased rates of diagnosis of various non–SARS-CoV-2 infections in the 12 months following an acute SARS-CoV-2 infection, even if the initial infection is mild to moderate.

They also found that patients hospitalized for COVID-19 infections were at greater risk for other infections in the year after illness, compared to patients who were hospitalized for influenza.

❦ Almost 50% higher rate of non-COVID respiratory infections

Compared with the test-negative control group, participants with a positive COVID-19 test who were not admitted had significantly increased rates of outpatient diagnosis of bacterial, fungal, and viral infectious illnesses (increased risk of 17%), outpatient respiratory infections (increased risk of 46%), and admission to hospital for infectious illnesses (increased risk of 41%), including for sepsis and respiratory infections.

Overall, non-hospitalized COVID patients had higher rates in 32% of the 65 laboratory-based outcomes compared to those who tested negative for SARS-CoV-2.

That rate jumped in hospitalized COVID-19 patients, who had higher rates of positive results in 71% of the examined laboratory tests, after accounting for multiple comparisons with the COVID-negative cohort.

❦ COVID may alter immune function

To further analyze the association between COVID-19 and subsequent infections, the authors compared people admitted to the hospital for seasonal influenza (3,293) and those admitted for COVID-19 (12,450) in the VA database, and found that COVID patients had higher rates of admission to hospital for infectious illnesses (increased risk of 24%), admission to hospital for sepsis (increased risk of 35%), and in-hospital use of antimicrobials (increased risk of 23%).

“These findings have important implications for understanding the potential impact of COVID-19 on long-term immune function and susceptibility to pathogens,” Chodick writes in a Lancet Comment on the study.

“The evidence suggests effects extending beyond the acute phase of infection, affecting even mild cases.”’

❂

�� (2 Apr 2025 ~ CIDRAP) COVID-19 may put patients at risk for other infections for at least 1 year ➤

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�� (1 Apr 2025 ~ The Lancet: Infectious Diseases) ‘ Rates of infection with other pathogens after a positive COVID-19 test versus a negative test in US veterans (November 2021 to December 2023): a retrospective cohort study ’.

❦ Study ~ ‘ Rates of infection with other pathogens after a positive COVID-19 test versus a negative test in US veterans (November 2021 to December 2023): a retrospective cohort study ’

By Cai et al / The Lancet: Infectious Diseases ( 1 Apr 2025 )

‘In the 12 months of follow-up, compared with participants who had a negative test for COVID-19, people with COVID-19 who did not require admission to hospital during the acute phase of infection had increased test positivity rates for bacterial infections (in blood, urine, and respiratory cultures) and viral diseases (including Epstein–Barr virus , herpes simplex virus reactivation , and respiratory viral infections ).

People who were positive for COVID-19 and admitted to hospital also had increased rates of bacterial infections in blood, respiratory, and urine biospecimens, and viral infections in blood and respiratory biospecimens.

Analyses of pre-specified outcomes showed that, compared with the test-negative control group, participants with a positive COVID-19 test who were not admitted to hospital had significantly increased rates of outpatient diagnosis of infectious illnesses (increased risk of 17% ), including bacterial , fungal , and viral infections ; outpatient respiratory infections (increased risk of 46% ); and admission to hospital for infectious illnesses (increased risk of 41% ), including for sepsis and respiratory infections ; the rates of pre-specified outcomes were generally higher among those who were admitted to hospital for COVID-19 during the acute phase.

❦ COVID-19 vs. seasonal influenza

Compared with people admitted to hospital for seasonal influenza , those admitted for COVID-19 had higher rates of admission to hospital for infectious illnesses (increased risk of 24% ), admission to hospital for sepsis (increased risk of 35% ), and in-hospital use of antimicrobials (increased risk of 23% ).’

❂

�� (1 Apr 2025 ~ The Lancet: Infectious Diseases) Rates of infection with other pathogens after a positive COVID-19 test versus a negative test in US veterans (November 2021 to December 2023): a retrospective cohort study ➤

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�� (1 Apr 2025 ~ The Lancet: Infectious Diseases ~ Comment) ‘ Long-term infectious sequelae after SARS-CoV-2 infection should be considered in mild cases too ’.

❦ Comment ~ ‘ Long-term infectious sequelae after SARS-CoV-2 infection should be considered in mild cases too ’

By Gabriel Chodick / The Lancet: Infectious Diseases ~ Comment ( 1 Apr 2025 )

❦ ‘Cai and colleagues contribute important insights into a previously under-explored consequence: the elevated rates of subsequent infections following SARS-CoV-2 infection , including in people who had not been admitted to hospital for COVID-19 or developed post-COVID-19-condition (also known as long COVID).

To establish whether these increased infection rates were unique to SARS-CoV-2, Cai and colleagues conducted comparative analyses with patients who were admitted to hospital for influenza.

Patients admitted to hospital for COVID-19 showed higher rates of all-cause admissions to hospital and infectious illness-related hospitalisations , including sepsis and positive urine and blood cultures , compared with patients admitted to hospital for influenza.

These findings complement a previous VA cohort study from the same group, which showed 51% greater all-cause mortality hazard in the COVID-19 group versus the influenza group.

A key advancement of Cai and colleagues’ study is the identification of increased infection rates among patients who were not admitted to hospital [for COVID-19] .

‘While previous research has primarily shown elevated rates of infection in patients with long-COVID, or in those requiring admission to hospital, this analysis demonstrates substantial increases in infection rates even in those with mild initial disease .’

This builds upon another analysis of VA healthcare data, which showed increased rates of various non-communicable conditions in patients with COVID-19 who were not admitted to hospital , including pulmonary diseases , hyperglycemia , diabetes , kidney disease , and gastrointestinal complications .

‘These findings have important implications for understanding the potential impact of COVID-19 on long-term immune function and susceptibility to pathogens .

The evidence suggests effects extending beyond the acute phase of infection, affecting even mild cases .’

This growing body of research on post-acute COVID-19 sequelae supports a bi-directional relationship between non-communicable diseases and infectious diseases , resulting in persistently increased risk of adverse outcomes in the months and years after initial SARS-CoV-2 infection .’

❂

�� (1 Apr 2025 ~ The Lancet: Infectious Diseases ~ Comment) Long-term infectious sequelae after SARS-CoV-2 infection should be considered in mild cases too ➤

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More... Immunity

More... PASC (‘Long COVID’)

Beyond Long COVID – How reinfections could be causing silent long-term organ damage

Thu, 20 Mar 2025 15:10:33 GMT

CBC Radio-Canada interview with long COVID [PASC] researcher David Putrino from the Icahn School of Medicine at Mount Sinai in New York.

�� (20 Mar 2025 ~ Radio-Canada / Canadian Broadcasting Corporation) ‘ Beyond long COVID – how reinfections could be causing silent long-term organ damage ’.

❂

❦ Radio interview ~ ‘Beyond long COVID – how reinfections could be causing silent long-term organ damage’

David Putrino interviewed by Bob McDonald .

Produced by Sonya Buyting for the Canadian Broadcasting Corporation ( 20 Mar 2025 )

❦ ‘COVID may no longer be considered an official global emergency, but mounting scientific evidence suggests every COVID infection a person gets increases their risk of developing long-term health issues.

The long-term effects can show up as long COVID , with symptoms such as shortness of breath, digestive problems, fast or irregular heartbeats, extreme fatigue and ‘brain fog’, or as silently-accumulating cellular or organ damage.

“There is no such thing as a COVID infection without consequence,” says long COVID researcher, David Putrino, from the Icahn School of Medicine at Mount Sinai in New York.

Putrino has been studying the lingering effects of COVID since early in the pandemic five years ago.

“There is more and more literature emerging to show that, beyond long COVID, there are also effects that SARS-CoV-2 infections are having on the bodies of the general public that manifest in a way that might be viewed as silent. So what I mean by that is no-one’s going to their doctor and saying “I feel different” or “I feel as though my functional status has changed,” but what’s happening is, silently in the background, things are changing.

A good example of that is the effect that SARS-CoV-2 infections can have on cognition .

“There was a recent 2024 study showing us that individuals who survive an acute COVID-19 infection – these are not individuals who are getting diagnosed with long COVID – on average will lose somewhere in the neighbourhood of two to six IQ points per infection .”

So there is a cumulative effect that can be occurring with each infection.

Early in the pandemic, we actually published a paper where we showed that, even in animal models — when we infected mice with a very, very mild case of SARS-CoV-2 infection — which only caused lung inflammation, we still saw these inflammatory chemicals called chemokines emerging from the infected lungs and starting to attack central nervous system structures such as the spinal cord and the brain.

“This is a virus that, once it enters the body, is very capable of entering the bloodstream , creating immune responses that travel all over the body .”

In all of the peer-reviewed literature that has emerged on long COVID , we’ve seen that it is a very diffuse clinical syndrome where every single organ system can be affected. And at last count, over 200 symptoms have been catalogued as potential symptoms of long COVID.

When we actually dig into the science of why long COVID is causing the symptoms that it’s causing, we see that there are problems such as what we call ‘ viral persistence ’.

Meaning the SARS-CoV-2 virus is not being effectively cleared by the body and it’s sticking around.

It’s hiding out in different areas of the body in what we typically call ‘immune privileged sites’, which mean that immune cells don’t actually go there and can’t ‘seek out’ and destroy the virus. That can happen in a number of different locations in the body, which leads to a wide array of symptoms.

We also see that the virus can cause prolonged chronic inflammation that can be whole-body wide. So it can affect every single organ and so often, many of the symptoms that people are experiencing are more related to which organ is most susceptible to them given their past medical history.

We see things that are quite insidious. People who were pre-diabetic are suddenly diabetic. People who were having a few issues with their gallbladder suddenly can’t digest fat anymore.

In 2021, two colleagues of mine published a really wonderful paper that I think is very prescient and it spoke about why SARS-CoV-2 presents such an increased threat to cause persistent symptoms. The reality of that situation is that this virus has a lot of very unique qualities that specifically cause immune damage to the host.

So it’s not just about infecting you and causing respiratory illness and fever, and all of the things that we usually get with the viral infection. This virus also specifically causes your immune system to become weaker.

“This virus also specifically causes your immune system to become weaker .”

It disrupts what we call ‘interferon signalling’, which is part of the immune system that helps you to fight off infections or latent infections, such as Epstein Barr virus .

Typically our immune system can keep these things suppressed, but when SARS-CoV-2 enters the picture, it starts to cause altered interferon signalling. It causes immune damage and dysregulation.

And suddenly, not only does your body have trouble clearing the SARS-CoV-2 virus itself, but it also starts to have trouble keeping some of these other viruses that have been latent from reactivating and causing problems.

In addition to SARS-CoV-2’s ability to dysregulate the immune system and suppress the immune system, the spike protein itself is very damaging to blood vessel structures as well as red blood cells and platelets themselves.

“And so between those two features, the ability to dysregulate the immune system and the ability to cause systemic damage throughout the bloodstream , you have a very dangerous novel virus on your hands.”

In 2023, we published a paper in Nature where we showed that individuals with long COVID were much more likely than a cohort of healthy controls to express signs of what we call ‘T-cell exhaustion’. Meaning that their T cells, which are parts of the immune system that are typically used to fight off infections, are starting to present as exhausted – that there has been a persistent stimulation of these T cells for long enough that their responses over time are starting to weaken.

As a result, in this study we saw immune dysregulation, we saw hormonal dysregulation, we saw reactivation of herpes viruses that were previously thought to be latent.

And as we have made leaps and bounds in our ability to understand the role of these persistent pathogens, these things that we used to think, “Everybody’s got Epstein-Barr virus, but don’t worry, it sort of just lays dormant in your body and it doesn’t cause any trouble.”

What we’re learning is that it very much can cause trouble. If it’s mixed with another pathogen [such as SARS-CoV-2], and that pathogen causes the reactivation, then people can get very, very sick.

For the longest time in the field of immunology, there was the sort of adage that your immune system needs to be tested every now and again to stay strong. That’s an old-fashioned idea.

The more new-fashioned and evidence-based idea is that, although your immune system can take on [a COVID] infection, you want to avoid testing it as much as possible because your body is sustaining damage with each infection that it survives.”

❂

�� (20 Mar 2025 ~ Canadian Broadcasting Corporation) ‘ Beyond Long COVID – How reinfections could be causing silent long-term organ damage ➤ ’.

“ If y’all are busy weakening your immune systems with one virus, let me assure you that there are packs of other pathogens out there waiting to chew on the leftovers. ”

❂

More... Reinfection & Immunity

More... PASC (‘Long Covid’)

📖 Does Covid Lead to Dementia? What We Know About Covid’s Impact on Your Brain

Mon, 03 Mar 2025 10:53:47 GMT

‘For patients already battling Alzheimer’s disease, studies indicate that Covid can exacerbate brain inflammation, damage immune cells, and accelerate the disease.

Even previously healthy older adults face an increased risk of cognitive impairment and new-onset dementia after infection.

Mild Covid cases in younger adults have also been linked to brain issues affecting memory and thinking. ’

�� (3 Mar 2025 ~ Bloomberg UK) ‘ What We Know About Covid’s Impact on Your Brain ’.

❦ Financial media article ~ ‘What We Know About Covid’s Impact on Your Brain’

By Jason Gale / Bloomberg UK ( 3 Mar 2025 )

❦ ‘Five years after the pandemic began, researchers are increasingly recognizing the toll Covid can take on brain health.

Many of those who have had the disease struggle with persistent issues such as brain fog , depression and cognitive slowing , hindering their ability to work and otherwise function.

Scientists have found that those who have had Covid are more likely to have elevated levels in their blood of the same proteins that are prevalent in people with Alzheimer’s disease .

Researchers are concerned that the findings could be early warning signs of a future surge in cases of dementia and other neurodegenerative conditions, prolonging Covid’s societal, economic , and health burden.

❦ What do studies show about Covid and the brain?

In 2021, UK researchers reported early results from a study comparing brain scans taken before and after the pandemic began.

They discovered signs of damage and accelerated aging in the brain, particularly in the part responsible for smell – even in patients who had experienced mild cases of Covid months earlier.

Research has since shown that Covid-related cognitive deficits can persist for years , especially in older adults and those who suffered from more severe cases.

For instance, a study of people aged 60 or older who were hospitalized during China’s first Covid wave showed that 2 1/2 years later, 40% developed cognitive impairment , compared with just 14% of their uninfected spouses.

A 2024 UK study of people hospitalized for Covid treatment concluded that as a group they showed a significant worsening of psychiatric and cognitive symptoms two to three years after their discharge.

At that stage, half experienced moderate to severe depression, a quarter suffered severe cognitive decline, and one in nine showed a loss of mental function equivalent to a 30-point drop on the IQ scale , where a score of 100 is average.

‘ For patients already battling Alzheimer’s disease , studies indicate that Covid can exacerbate brain inflammation , damage immune cells , and accelerate the disease .

Even previously healthy older adults face an increased risk of cognitive impairment and new-onset dementia after infection. ’

For patients already battling Alzheimer’s disease , studies indicate that Covid can exacerbate brain inflammation, damage immune cells, and accelerate the disease .

Even previously healthy older adults face an increased risk of cognitive impairment and new-onset dementia after infection. Mild Covid cases in younger adults have also been linked to brain issues affecting memory and thinking .

These symptoms typically fluctuate and tend to worsen after physical or mental exertion , often impairing the ability of individuals to work and socialize.

A February 2024 study of nearly 113,000 people found greater loss of memory and executive function among people who had been infected at some point by the SARS-CoV-2 virus that causes Covid compared with those who had never had it.

People who were struck later in the pandemic had smaller deficits compared with those infected with either the original or the alpha strain, the first variant of the virus to come to researchers’ attention.

‘The same study found that even mild cases of Covid led to cognitive decline , equivalent to an average 3-point drop in IQ .

For those with unresolved symptoms such as persistent shortness of breath or fatigue, the decline amounted to a 6-point decrease in IQ . ’

UK scientists reported subtle but persistent cognitive effects in a so-called human challenge study published in September 2024.

For the research, 34 healthy volunteers ages 18 to 30 completed 11 tasks on an iPad during two consecutive days before they were deliberately exposed to the original SARS-CoV-2 strain.

Roughly half the group developed an infection. None of the participants noticed any cognitive effects after their initial exposure to the coronavirus.

‘However, six further rounds of testing found the infected group had measurable reductions in memory and executive function compared with those who weren’t infected, with the differences still evident a year after the experiment.’

Studies also suggest that neurological and neurocognitive symptoms – such as headaches , confusion , and brain fog – may be more common among female long Covid patients than their male counterparts, highlighting potential sex-based differences in the virus’s long-term impact on the brain.

Some evidence suggests an infection may increase the risk of Parkinson’s disease .

This link is supported by the rise in cases of parkinsonism – a collection of symptoms such as tremors , slow movement , stiffness and balance issues – following a case of Covid.

❦ How many people are affected?

There is no robust global data on the number of people experiencing prolonged neurocognitive symptoms after a bout of Covid.

A 2022 population-based study in the Netherlands estimated that long Covid affects about one in eight people after infection, with vaccination only partially reducing the risk.

By 2024, the condition was estimated to have afflicted around 400 million people worldwide, with brain fog as a primary symptom .

While some people recover over time, a 2025 study found about 4.5% of infected adults may develop myalgic encephalomyelitis (also known as chronic fatigue syndrome ), a debilitating and often long-term condition characterized by worsening symptoms after physical or mental exertion, unrefreshing sleep, and either cognitive impairment or dizziness when standing.

Different studies have found that anywhere from 7% to 59% of people still have problems with thinking and memory three months after recovering from Covid, according to one review of the research.

❦ How does Covid harm the brain?

The effects of a SARS-CoV-2 infection on the brain are the focus of intense research and remain only partially understood.

A study published in January by scientists at Imperial College London found that Covid survivors were more likely to have elevated levels of beta amyloid and tau-181 – proteins linked to Alzheimer’s disease – in their blood.

These findings suggest that a case of Covid could heighten the future risk of developing the disease.

Other studies suggest that during acute infection, the virus may damage nerves , particularly in the olfactory bulb – which transmits smell impulses to the brain.

This damage could lead to long-lasting issues, with the virus potentially infecting the brain through this pathway, altering its structure and resulting in impaired cognition and fatigue .

Persistent viral remnants or the initial infection itself may trigger neuroinflammation and disrupt the immune system , causing antibodies and T cells to mistakenly attack healthy brain cells, damage blood vessels , and harm the blood-brain barrier.

A study published in late 2024 found that the virus’s spike protein can linger in the body for years after infection, particularly in areas around the skull and brain , potentially contributing to the neurological symptoms of long Covid.

Additional research points to blood clots as potential drivers of damage to nerve cells and restricted oxygen and nutrient supply to the brain.

A SARS-CoV-2 infection during pregnancy – particularly in mothers who were unvaccinated or had no prior infection – may also increase the risk of neurodevelopmental delays in their offspring, though scientists are still working to understand the extent of this risk amid inconsistent findings.

❦ What is the possible economic impact?

While the long-term effects of Covid on conditions such as Parkinson’s disease and dementia remain uncertain, the stakes are high.

These are both lifelong, incurable, progressive illnesses with a profound societal impact, affecting not only those diagnosed but also their families, caregivers and the broader healthcare system.

Already, there are significant economic repercussions globally from the enduring prevalence of long Covid . Analysts have put the annual economic toll at between $864 billion and $1.04 trillion in developed nations alone – roughly 1% of the global economy .

Much of the impact stems from on-going disability and illness, with persistent fatigue and concentration problems among the most common conditions.

‘ Long Covid has disproportionately affected younger adults in their prime . ’

Long Covid has disproportionately affected younger adults in their prime – those who drive much of the workforce, productivity and innovation – exacerbating labor shortages and straining economic growth.’

❂

❦ Related information

Related explainers on long Covid and Covid vaccine safety .
Neurologists Serena Spudich and Avindra Nath outline the nervous system consequences of Covid.
Neurologist Michelle Monje talks about the effects of long Covid on the brain .
Epidemiologist Ziyad Al-Aly discusses how Covid leaves its mark , and global biosecurity expert Raina MacIntyre and colleagues look at its after-effects in Australia .

❂

�� (3 Mar 2025 ~ Bloomberg UK) ‘What We Know About Covid’s Impact on Your Brain ’.

Legend: ‘Younger Americans Report More Cognitive Disability’ .

‘Prevalence of adults experiencing serious difficulty concentrating, remembering, or making decisions.

Rates have increased among US adults ages 18-44 years since Covid-19 emerged .’ ➤

�� (3 Mar 2025 ~ Bloomberg UK) What We Know About Covid’s Impact on Your Brain ➤

❂

More... Dementia & the Brain

More... PASC (‘Long Covid’)

☰ The beating heart... 70 studies & articles on SARS-CoV-2 and the cardiovascular system (2020–2023/2024)

Fri, 28 Feb 2025 20:32:46 GMT

‘But even people who had not been hospitalized had increased risks of many conditions, ranging from an 8% increase in the rate of heart attacks to a 247% increase in the rate of heart inflammation.’

Nature (2 Aug 2022)

‘Either symptomatic or asymptomatic SARS-CoV-2 infection is associated with increased risk of late cardiovascular outcomes and has causal effect on all-cause mortality in a late post-COVID-19 period.’

The American Journal of Cardiology (15 Sep 2023)

�� (2 Mar 2022 ~ JAMA) ‘The COVID Heart – One Year After SARS-CoV-2 Infection, Patients Have an Array of Increased Cardiovascular Risks’. ➲

‘ Patients with COVID-19 were at increased risk of a broad range of cardiovascular disorders including cerebrovascular disorders, dysrhythmias, ischemic and non-ischemic heart disease, pericarditis, myocarditis, heart failure and thromboembolic disease. ’

�� (19 Mar 2024 ~ European Society of Cardiology: Cardiovascular Research) ‘Persistent increase of cardiovascular and cerebrovascular events in COVID-19 patients: a 3-year population-based analysis’. ➲

‘ The increase of cardiovascular risk associated with COVID-19 might be extended for years and not limited to the acute phase of the infection. ’

�� (14 Mar 2022 ~ Johns Hopkins) ‘COVID and the Heart: It Spares No-One’. ➲

‘ New evidence has revealed that anyone infected with COVID is at higher risk for heart issues – including clots, inflammation, and arrhythmias – a risk that persists even in relatively healthy people long after the illness has passed. ’

�� (23 Feb 2023 ~ Journal of Neurology) ‘Patterns of acute ischemic stroke and intracranial hemorrhage in patients with COVID-19’. ➲

‘ 220 patients (49.8%) presented with respiratory symptoms, and 167 (37.8%) presented with neurological symptoms first.

Acute ischemic stroke (AIS) was detected in 70 (15.8%), and intracranial hemorrhage (IH) in 48 (10.9%) patients.

There was no association between AIS or IH and the severity of COVID-19. ’

�� (22 Jun 2023 ~ British Heart Foundation) ‘Nearly 100,000 more deaths involving heart conditions and stroke than usual since pandemic began’. ➲

‘ Nearly 100,000 more people with cardiovascular disease than expected have died since the start of the pandemic in England. ’

�� (4 Aug 2022 ~ Fortune) ‘Blood clots, heart problems, kidney failure: COVID creates a higher risk for rare pediatric health problems, new CDC study finds’. ➲

‘ Children and teens who’ve had COVID are at greater risk for blood clots, heart problems, kidney failure, and Type 1 diabetes. ’

�� (2 Aug 2022 ~ Nature: News) ‘Heart disease after COVID: what the data say’. ➲

‘ But even people who had not been hospitalized had increased risks of many conditions, ranging from an 8% increase in the rate of heart attacks to a 247% increase in the rate of heart inflammation. ’

�� (7 Feb 2022 ~ Nature: Medicine) ‘Long-term cardiovascular outcomes of COVID-19’. ➲

‘ Our results provide evidence that the risk and 1-year burden of cardiovascular disease in survivors of acute COVID-19 are substantial. ’

�� (3 Mar 2023 ~ JAMA) ‘One-Year Adverse Outcomes Among US Adults With Post-COVID-19 Condition vs Those Without COVID-19 in a Large Commercial Insurance Database’. ➲

‘ Results from this study indicated a statistically significant increased risk for a range of cardiovascular conditions as well as mortality.

While these risks were heightened for individuals who experienced a more severe acute episode of COVID-19 (ie. requiring hospitalization), it is essential to note that most individuals (72.5%) in the cohort did not experience hospitalization during the acute phase.

Many of these conditions will have lasting effects on quality of life. ’

�� (10 Feb 2022 ~ Nature: News) ‘Heart-disease risk soars after COVID – even with a mild case’. ➲

‘ Heart-disease risk soars after COVID – even with a mild case: Massive study shows a long-term, substantial rise in risk of cardiovascular disease, including heart attack and stroke, after a SARS-CoV-2 infection. ’

�� (24 Apr 2020 ~ The Washington Post / The Seattle Times) ‘Healthy people in their 30s and 40s, barely sick with COVID-19, are dying from strokes’. ➲

‘[Physician-researcher] Mocco, who has spent his career studying strokes and how to treat them, said he was “completely shocked” by the analysis.

He noted the link between COVID-19 and stroke “is one of the clearest and most profound correlations I’ve come across”. ’

�� (1 Nov 2021 ~ Harvard Medical School) ‘COVID-19 diagnosis raises risk of heart attack, stroke’. ➲

‘ In the week after a COVID-19 diagnosis, the risk of a first heart attack increased by three to eight times.

The risk of a first stroke caused by a blood clot multiplied by three to six times. ’

�� (31 Jan 2022 ~ University of Utah) ‘COVID-19 Increasing Stroke Risks in People of All Ages’. ➲

‘ “We are definitely seeing a huge increase in younger stroke survivors who are post-COVID diagnosis,” Kinzinger says. “We know that vascular complications go along with COVID infections, which can lead to strokes and other cardiovascular issues.” ’

�� (10 Jan 2023 ~ Frontiers in Cardiovascular Medicine) ‘SARS-CoV-2 infection predicts larger infarct volume in patients with acute ischemic stroke’. ➲

‘ Hypercoagulation and microthrombosis represent the typical features of COVID-19 caused by SARS-CoV-2 [ infection ] .

The pathogenic mechanisms are not yet fully understood, but multiple pathways are involved, including endothelialitis * .

The relative risk for the occurrence of AIS [ a cute ischemic stroke ] is 3- to 4-fold greater compared to that of non-infected hospitalized historical or contemporary control cohorts, and since the outcome of AIS patients with COVID-19 appear worse both in terms of initial stroke severity and functional outcome/mortality, this subgroup of infected patients deserves particular attention. ’

* Note : Endothelialitis refers to the inflammation of the endothelial cells that line the endothelium , which is the inner lining of blood vessels .

�� (30 Aug 2022 ~ The Financial Times) ‘The growing evidence that Covid-19 is leaving people sicker: The potential impact on heart and brain disease poses challenges to healthcare systems globally’. ➲

‘ Researchers found that rates of many conditions, such as heart failure and stroke, were substantially higher in people who had recovered from Covid than in similar people who had not been infected.

Although the evidence is still coming into focus, it is already becoming clearer to clinicians and health leaders in medical systems around the world that they are coping with a higher burden of disease in the population. ’

�� (4 Jun 2020 ~ Science Daily) ‘Coronavirus linked to stroke in otherwise healthy young people’. ➲

‘ Young patients with no risk factors for stroke may have an increased risk if they have contracted COVID-19, whether or not they are showing symptoms of the disease. ’

�� (24 Aug 2022 ~ Nature: News) ‘Could tiny blood clots cause long COVID’s puzzling symptoms?’ ➲

‘ Researchers already know that people with COVID-19, especially severe disease, are more likely to develop clots. The virus can infect cells lining the body’s 100,000 kilometres of blood vessels, causing inflammation and damage that triggers clotting. ’

�� (Sep 2020 ~ The Lancet) ‘COVID-19 related stroke in young individuals’. ➲

‘ We believe that, in otherwise healthy, young patients who present with stroke during the pandemic, the diagnosis of COVID-19 should be thoroughly investigated. ’

�� (9 Feb 2022 ~ Science) ‘COVID-19 takes serious toll on heart health – a full year after recovery: Giant study shows striking rise in long-term heart and vessel disease’. ➲

‘ The results are “stunning… worse than I expected, for sure,” says Eric Topol, a cardiologist at Scripps Research.

“All of these are very serious disorders… If anybody ever thought that COVID was like the ‘flu, this should be one of the most powerful data sets to point out that it’s not.”

“In the post-COVID era, COVID might become the highest risk factor for cardiovascular outcomes,” greater than well-documented risks such as smoking and obesity, says Larisa Tereshchenko, a cardiologist and biostatistician at the Cleveland Clinic. ’

�� (15 Sep 2023 ~ The American Journal of Cardiology) ‘Risk of Cardiovascular Events After COVID-19’. ➲

‘ Either symptomatic or asymptomatic SARS-CoV-2 infection is associated with increased risk of late cardiovascular outcomes and has causal effect on all-cause mortality in a late post-COVID-19 period. ’

�� (21 Feb 2022 ~ The Washington Post) ‘Five months post-covid, Nicole Murphy’s heart rate is still doing strange things’. ➲

‘ Indeed, as the months since their infections have turned into years, people who initially had mild or even some asymptomatic coronavirus cases are pouring into cardiology practices across the country. ’

�� (1 Apr 2022 ~ Weill Cornell Medicine) ‘Are COVID-19-Linked Arrhythmias Caused by Viral Damage to the Heart’s Pacemaker Cells?’ ➲

‘ The SARS-CoV-2 virus can infect specialized pacemaker cells that maintain the heart’s rhythmic beat, setting off a self-destruction process within the cells, according to a pre-clinical study. ’

�� (23 Sep 2020 ~ Science) ‘COVID-19 can affect the heart: COVID-19 has a spectrum of potential heart manifestations with diverse mechanisms’. ➲

‘ Collectively, these young, healthy individuals had mild COVID-19 but were subsequently found to have unsuspected cardiac pathology. ’

�� ( Updated: 12 May 2023 ~ The British Heart Foundation) ‘Is coronavirus a disease of the blood vessels?’ ➲

‘ By triggering endothelial damage, coronavirus infection may cause abnormal blood clotting, ‘leaky’ vessels and reduced blood flow. These endothelial effects could have consequences from head to toe.

In the lungs, these effects can cause clots and fluid to accumulate, which means the lungs are less able to get oxygen into the body.

In the brain, damage to endothelial cells in the blood-brain barrier could lead to inflammation.

In the limbs, reduced blood flow could lead to “Covid toe”. ’

�� (17 Oct 2022 ~ Nature: Acta Pharmacologica Sinica) ‘Endothelial dysfunction in COVID-19: an overview of evidence, biomarkers, mechanisms and potential therapies’. ➲

‘ It has been increasingly appreciated that COVID-19 is not only an infectious disease involving the lung; but also, a vascular disease affecting extrapulmonary organs.

Endothelial dysfunction-induced endotheliitis/endothelialitis/endotheliopathy following SARS-CoV-2 infection arises from a plethora of physiopathological mechanisms, including both direct mechanism or indirect mechanisms. ’

�� (7 Feb 2022 ~ Massachusetts General Hospital / Science Daily) ‘COVID-19-associated strokes link to higher disability and death risk, study finds’. ➲

‘ The data suggest that patients from less affluent areas may have been at greater risk for serious complications such as stroke because of their inability to carry out protective measures such as social distancing or working at home. ’

�� (15 Mar 2022 ~ Thomas Jefferson University) ‘International Multi-Center Study Confirms Stroke Risk in Younger Healthier COVID-19 Patients’. ➲

‘ The stroke patients who tested positive for COVID-19 were often younger, had multiple large vessels blocked, and often had worse outcomes than our usual patients. This international study confirms those early, alarming observations. ’

�� (16 Aug 2022 ~ Penn Medicine News) ‘People with Severe COVID-19 Face Increased Risk of Life-Threatening Blood Clots’. ➲

‘ “Our research found this association both before and during vaccine availability, showing that the risk was not stemming from vaccination,” said Vincent Lo Re III, MD, MSCE, an associate professor of Infectious Diseases and Epidemiology at Penn. ’

�� (6 Apr 2022 ~ The Guardian) ‘Covid linked to 33-fold increase in risk of potentially fatal blood clot: Infection with virus also associated with fivefold increase in risk of deep vein thrombosis, data suggests’. ➲

‘ Although the risks were highest in patients with more severe illness, even those with mild Covid had a threefold increased risk of DVT and a sevenfold increased risk of pulmonary embolism. ’

�� ( Updated: 16 Dec 2024 ~ The British Heart Foundation) ‘How does Covid-19 affect your heart?’ ➲

‘ Research suggests that Covid-19 can increase the risk of heart and circulatory conditions, like heart attack and stroke, after infection.

Damage can lead to abnormal blood clotting, ‘leaky’ blood vessels and reduced blood flow. Covid-19 can also lead to inflammation of the heart muscle (myocarditis) and heart lining (pericarditis).

Some research suggests that Covid-19 could be linked to an increased risk of developing high blood pressure (hypertension). This is a serious condition, as high blood pressure raises your chances of having a heart attack or stroke. ’

�� (8 Sep 2022 ~ MedPage Today) ‘Inflammation a Culprit in Long COVID Heart Problems: Prospective study illuminates mechanisms of lingering heart issues after mild COVID-19’. ➲

‘ Their study included only patients without previously known cardiac conditions, comorbidities, or abnormal lung function tests at the baseline assessment and who had not been hospitalized for acute COVID-19 at any point. ’

�� (5 Sept 2022 ~ Nature: Medicine) ‘Long-term cardiac pathology in individuals with mild initial COVID-19 illness’. ➲

‘ Baseline measurements from 346 individuals with COVID-19 (52% females) were obtained at a median of 109 days after infection, when 73% of participants reported cardiac symptoms, such as exertional dyspnea (62%), palpitations (28%), atypical chest pain (27%) and syncope (3%).

At follow-up (329 days after infection), 57% of participants had persistent cardiac symptoms.

Female gender and diffuse myocardial involvement on baseline imaging independently predicted the presence of cardiac symptoms at follow-up. ’

�� (26 Sep 2022 ~ Nature: Medicine) ‘Lingering cardiac involvement in previously well people after mild COVID-19’. ➲

‘ In this article, the authors report a novel association between heart inflammation and prolonged shortness of breath, palpitations and chest pain, which are common after mild COVID-19. ’

�� (19 Sep 2022 ~ American Heart Association) ‘Association of COVID-19 With Major Arterial and Venous Thrombotic Diseases: A Population-Wide Cohort Study of 48 Million Adults in England and Wales’. ➲

‘ Associations between COVID-19 and thrombotic events did not vary markedly by age or sex, but were greater in people of Black or Asian race than those of White race, and in people without than with a history of vascular events. ’

�� (28 Sep 2022 ~ Springer Nature) ‘Impaired left ventricular deformation and ventricular-arterial coupling in post-COVID-19: association with autonomic dysregulation’. ➲

‘ Subjects in the post-acute COVID-19 phase present autonomic dysregulation… and impaired heart rate variability, which are associated with central aortic stiffness, ventricular-arterial impairment, and left ventricular function impairment. ’

�� (29 Sep 2022 ~ Brisbane Times) ‘Unlike flu, COVID-19 attacks DNA in the heart: new research’. ➲

‘ Rather than extreme inflammation which they had expected to find, inflammation signals had been suppressed in the hearts of the COVID-19 patients, while markers for DNA damage and repair were much higher than in people who had died from the ’flu.

The way the DNA damage presented was similar to the way chronic diseases such as diabetes or even cancer presented, with the tissues of the heart putting out DNA damage signals. ’

❦ Study : ‘ Transcriptomic profiling of cardiac tissues from SARS-CoV-2 patients identifies DNA damage ’ by Kulasinghe & Liu et al / Immunology (15 Sep 2022) ➲

�� (6 Oct 2022 ~ Fortune) ‘Strokes, heart attacks, sudden deaths: Does America understand the long-term risks of catching COVID?’ ➲

‘ Significantly, the risk of some of these complications is stronger in younger adults.

As the virus becomes more immune-evasive, our arsenal is shrinking, not expanding, despite what the CDC [ the USA’s Centers for Disease Control ] and political leaders may claim. ’

�� (21 Apr 2021 ~ American Heart Association) ‘SARS-CoV-2 and Stroke Characteristics: A Report From the Multinational COVID-19 Stroke Study Group’. ➲

‘ 36% of the AIS [ Arterial Ischemic Stroke ] patients in our study were less than 55 years of age, and 46% were less than 65 years of age.

These proportions are considerably higher than the population-based reports before the pandemic (12.9%–20.7%). ’

�� (4 Aug 2021 ~ The Journal of Applied Laboratory Medicine) ‘COVID-19: A Serious Vascular Disease with Primary Symptoms of a Respiratory Ailment’. ➲

‘ [ During SARS-CoV-2 infection, ] endothelial cells encompassing the intima [ the innermost layer ] in arteries, capillaries, veins and the endocardium bind the viral particles via their ACE2 receptors, and consequently become severely inflamed, damaged, and/or destroyed. ’

�� (24 Oct 2022 ~ Medical Xpress) ‘COVID-19 surges linked to spike in heart attacks’. ➲

‘ The spikes in heart attack deaths have tracked with surges of COVID-19 infection – even during the presumed less-severe Omicron phase of the pandemic.

Furthermore, the data showed the increase was most significant among individuals ages 25–44. ’

�� (29 Sep 2022 ~ Journal of Medical Virology) ‘Excess risk for acute myocardial infarction mortality during the COVID-19 pandemic’. ➲

‘ The trend of mortality suggests that age and sex disparities have persisted even through the recent Omicron surge, with excess AMI * -associated mortality being most pronounced in younger-aged adults. ’

* Note : AMI = Acute myocardial infarction , or heart attack .

�� (24 Oct 2022 ~ Bloomberg UK) ‘Covid-19 Tied to Higher Risk of Deadly Blood Clots in Large Study’. ➲

‘ Non-hospitalized Covid patients were 2.7 times more likely to develop dangerous clots called venous thromboembolisms and were more than 10 times more likely to die than individuals who avoided the disease. ’

�� (25 Oct 2022 ~ CNBC) ‘People who caught mild Covid had increased risk of blood clots, British study finds’. ➲

‘ [ P ] atients hospitalized with Covid were 28 times more likely to develop blood clots, 22 times more likely to suffer heart failure, and 17 times more likely to have a stroke, according to the study. ’

�� (24 Oct 2022 ~ British Medical Journal: Heart) ‘Cardiovascular disease and mortality sequelae of COVID-19 in the UK Biobank’. ➲

‘ Overall, available evidence supports a distinct mechanistic role for COVID-19 in driving higher VTE * rates which occurs across disease severities and extends beyond the early post-infection phase. ’

* Note : Venous thromboembolism (VTE) = refers to a blood clot that starts in a vein .

�� (27 Apr 2021 ~ JACC: Basic to Translational Science) ‘SARS-CoV-2 Infects Human Engineered Heart Tissues and Models COVID-19 Myocarditis’. ➲

‘ This study provides evidence that cardiomyocytes are a target of SARS-CoV-2 in the human heart, and support the conclusion that SARS-CoV-2 infection of cardiomyocytes and resultant… inflammation contribute to the cardiac manifestations of COVID-19. ’

�� (19 Nov 2022 ~ Pediatric Neurology) ‘SARS-CoV-2 Infection and Increased Risk for Pediatric Stroke’. ➲

‘ COVID-19 infection can lead to a delayed hyperinflammatory response…

Based on epidemiologic data, we hypothesize that there is likely a delay of at least one month from the timing of initial COVID-19 infection to the development of stroke.

Our study suggests that prior COVID-19 infection, but not acute infection, is correlated with a risk for stroke in the pediatric population.

The risk for stroke appears to be distinct from the risk for [ Multisystem Inflammatory Syndrome in Children/MIS-C ] . ’

�� (17 Oct 2022 ~ News Medical Life Sciences) ‘Asymptomatic COVID could potentially cause more complications in trauma patients’. ➲

‘ Compared with similar trauma patients who tested negative for COVID, positive asymptomatic COVID trauma patients had higher rates of myocardial infarction and cardiac arrest (3.2% vs 0.9%). ’

�� (20 Jan 2022 ~ Science) ‘Nervous system consequences of COVID-19’. ➲

‘ [ High-field MRI ] examination of brain tissue demonstrates microvascular damage in structures plausibly related to neurologic manifestations of COVID-19, consistent with endothelial activation and widespread vascular injury observed in other organs. ’

�� (12 Nov 2022 ~ Springer Nature) ‘Inflammation and vascular remodeling in COVID-19 hearts’. ➲

‘ We conclude that cardiac involvement in COVID-19 is an angiocentric macrophage-driven inflammatory process, distinct from classical anti-viral inflammatory responses, and substantially underappreciated by conventional histopathologic analysis.

A systematic follow-up of non-fatal COVID-19 and long-COVID cases [ would help detect ] post-acute cardiac symptoms and fibrotic remodeling also in mild cases of disease due to the irreversible alterations of the cardiac vasculature. ’

�� (8 Jul 2022 ~ American Heart Association) ‘Thromboinflammation: From Atherosclerosis to COVID-19’. ➲

‘ The activating interplay of thrombosis [ blood clotting ] and inflammation (thromboinflammation) has been established as a major underlying pathway, driving not only cardiovascular disease but also autoimmune disease and most recently, COVID-19.

Endothelial dysfunction and thromboinflammation have emerged early on as the key pathogenic mechanisms driving COVID-19 pathology…

COVID-19–specific coagulopathy is epitomized by elevated levels of [ several glycoproteins involved in blood clotting ] . ’

�� (26 Dec 2022 ~ Nature: Communications) ‘Transcriptional reprogramming from innate immune functions to a pro-thrombotic signature by monocytes in COVID-19’. ➲

‘ These results [ reflect ] hypercoagulability and acquired coagulopathies in patients with COVID-19, and suggest that monocytes from moderate COVID-19 patients upregulate a pro-thrombotic gene expression signature upon secondary SARS–CoV–2 sensing. ’

�� (2 Dec 2022 ~ Time) ‘Tiny Blood Clots May Be to Blame for Long COVID Symptoms, Some Researchers Say’. ➲

‘ [ Stellenbosch University Physiological Sciences’ Chair ] posits that lingering viral remnants may damage the cells that line the blood vessels, prompting the formation of inflammation and microclots, which could in turn make the immune system attack itself. ’

�� (23 Aug 2021 ~ Springer Nature) ‘Persistent clotting protein pathology in Long COVID/Post-Acute Sequelae of COVID-19 (PASC) is accompanied by increased levels of antiplasmin’. ➲

‘ Results presented in the current paper point to a significant failure in the fibrinolytic process [ enzymatic breakdown of intravascular fibrin in blood clots ] during COVID-19 and also in patients with lingering Long COVID/PASC symptoms. ’

�� (26 Dec 2022 ~ Journal of Clinical Medicine) ‘Mid- and Long-Term Atrio-Ventricular Functional Changes in Children after Recovery from COVID-19’. ➲

‘ 60% of children who recovered from asymptomatic or mildly symptomatic COVID-19 still exhibit mild subclinical systolic cardiac impairment after an average follow-up of 148 ± 68 days from disease onset. ’

�� (13 Jan 2023 ~ Nature Reviews: Microbiology) ‘Long COVID: major findings, mechanisms and recommendations’. ➲

‘ Cardiac MRI studies revealed cardiac impairment in 78% of 100 individuals who had a prior COVID-19 episode (investigated an average of 71 days after infection) and in 58% of participants with long COVID (studied 12 months after infection), reinforcing the durability of cardiac abnormalities. ’

�� (21 Jan 2023 ~ The Sydney Morning Herald) ‘Fatal heart attacks have surged in Australia. Here’s why’. ➲

‘ “COVID-19 infection worsens pre-existing heart conditions, and increases the risk of developing more than 20 heart conditions including heart attack, blood clots, heart failure and stroke,” [ Dr. Amanda Buttery, Heart Foundation of Australia ] said. ’

�� (28 Nov 2022 ~ The Medical Journal of Australia) ‘Associations between COVID‐19 and hospitalisation with respiratory and non‐respiratory conditions: a record linkage study’. ➲

‘ The incidence of hospitalisation with cerebral infarction [ ischemic stroke ] was twice as high after COVID‐19 onset as during the baseline period. Other investigators have estimated the risk of stroke to be 2–13 times as high for people with COVID‐19.

The pathophysiology of cerebrovascular involvement is unclear, but may be related to substantial endothelial disruption in highly vascularised organs such as the brain. ’

�� (19 Jan 2023 ~ European Society of Cardiology) ‘COVID-19 patients retain elevated risk of death for at least 18 months after infection’. ➲

‘ COVID-19 is associated with higher risks of cardiovascular disease and death in the short- and long-term, according to a study in nearly 160,000 participants.

Compared to uninfected individuals, the likelihood of COVID-19 patients dying was up to 81 times higher in the first three weeks of infection and remained five times higher up to 18 months later. ’

�� (25 Jan 2023 ~ SciTech Daily / American Heart Association) ‘COVID Toll: Big Jump in Cardiovascular-Related Deaths Reported by American Heart Association’. ➲

‘ COVID-19 has both direct and indirect impacts on cardiovascular health. As we learned, the virus is associated with new clotting and inflammation. ’

�� (13 Jan 2023 ~ Nature Reviews: Microbiology) ‘Long COVID: major findings, mechanisms and recommendations’. ➲

‘ The narrative that COVID-19 had only respiratory sequelae led to a delayed realization of the neurological, cardiovascular and other multisystem impacts of COVID-19. ’

�� (2 Feb 2023 ~ Nature Communications) ‘High-depth sequencing characterization of viral dynamics across tissues in fatal COVID-19 reveals compartmentalized infection’. ➲

‘ This lends credence to the hypothesis that direct infection may lead to the heart-related sequelae observed in some COVID-19 patients.

SARS-CoV-2 may establish a viral reservoir in these anatomical sites, leading to on-going tissue-specific pathology ’

�� (15 Feb 2023 ~ Journal of the American Heart Association) ‘Collagen‐Specific HSP47+ Myofibroblasts and CD163+ Macrophages Identify Profibrotic Phenotypes in Deceased Hearts With SARS‐CoV‐2 Infections’. ➲

‘ Cardiac fibrosis complicates SARS-CoV-2 infections and has been linked to arrhythmic complications in survivors.

[ Post-infection cardiac scarring may lead to ] enhanced arrhythmogenesis, and even sudden cardiac death. As such, COVID‐19–induced cardiac fibrosis may have critical long‐term public health implications for healthcare systems and policy makers. ’

�� (8 Mar 2023 ~ Journal of Clinical Medicine) ‘Long-Term Adverse Effects of Mild COVID-19 Disease on Arterial Stiffness, and Systemic and Central Hemodynamics: A Pre-Post Study’. ➲

‘ The finding that the longer the period from COVID-19 infection the worse the vascular impairment was surprising, as we expected inflammation burden associated with COVID-19 to decrease with time. ’

�� (19 May 2023 ~ EurekAlert) ‘International COVID-19 Registry uncovers increased incidence of clotting in heart attack patients with COVID-19’. ➲

‘ COVID-19 is a pro-inflammatory, clot-forming disease and we now see its effect in the coronary arteries…

These new insights point to the need for clinicians to be meticulous with blood thinning strategies, early interventions and patient follow-up. ’

�� (10 Aug 2023 ~ Associated Press) ‘COVID-19 took a toll on heart health and doctors are still grappling with how to help’. ➲

‘ Long COVID patients were about twice as likely to seek care for cardiovascular problems like blood clots, abnormal heartbeats or stroke in the year after infection, compared to similar patients who’d avoided COVID-19. — U.S. insurance database analysis. ’

�� (21 Aug 2023 ~ American Heart Association / Medical Xpress) ‘Analysis finds COVID-19 may trigger new-onset high blood pressure’. ➲

‘ An analysis of electronic medical records for more than 45,000 people found that COVID-19 infection was significantly associated with the development of high blood pressure, according to new research published in Hypertension . ’

�� (28 Sep 2023 ~ National Institutes of Health) ‘SARS-CoV-2 infects coronary arteries, increases plaque inflammation’. ➲

‘ SARS-CoV-2, the virus that causes COVID-19, can directly infect the arteries of the heart and cause the fatty plaque inside arteries to become highly inflamed, increasing the risk of heart attack and stroke, according to a study funded by the NIH. ’

�� (28 Sep 2023 ~ Nature: Cardiovascular Research) ‘SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary vessels’. ➲

‘ Our data establish that SARS-CoV-2 infects coronary vessels, inducing plaque inflammation that could trigger acute cardiovascular complications and increase the long-term cardiovascular risk. ’

�� (18 Oct 2023 ~ Nature: Cardiovascular Research) ‘SARS-CoV-2 infection boosts inflammation in atherosclerotic plaques’. ➲

‘ A post-mortem study reported that severe vascular injury, including microthrombosis, was nine times more prevalent in COVID-19 lungs than inpatients with influenza. ’

�� (18 Oct 2023 ~ Nature: Cardiovascular Research) ‘SARS-CoV-2 infection boosts inflammation in atherosclerotic plaques (Fig. 1: SARS-CoV-2 infects coronary vessel lesions)’. ➲

‘ SARS-CoV-2 induces a strong pro-atherogenic inflammatory response… This pro-inflammatory response may contribute to the instability of atherosclerotic plaques and the increased incidence of ischemic cardiovascular complications in patients. ’

�� (9 Nov 2023 ~ European Heart Journal) ‘Prior COVID-19 infection is associated with persistent and higher thrombus burden in acute coronary syndromes’. ➲

‘ Our findings suggest that COVID-19 infection may lead to persistent endothelial dysfunction and hypercoagulability, portending increased severity of coronary artery ectasia and coronary thrombosis even after recovery from the initial infection. ’

�� (18 May 2022 ~ American Medical Association) ‘3 tips for doctors trying to manage long COVID’s cardiac symptoms’. ➲

‘ As many as 10% to 30% may develop long COVID following SARS-CoV-2 infection. In these individuals, symptoms such as chest pain, shortness of breath, and palpitations draw attention to the cardiovascular system.

Patients with long COVID may experience other cardiac symptoms such as elevated blood pressure, tachycardia out of proportion to that expected for effort, and drops in oxygen saturation.

There is also a lack of data to help guide diagnosis, treatment and prognosis.

That is why a systematic approach to assist in the evaluation and management of long COVID is needed, especially since the evidence base is likely to evolve over time.

Patient-centered models of care are needed to address long COVID.

This requires co-ordination by multi-disciplinary teams that include primary care physicians , sub-specialists such as pulmonologists , cardiologists , and neurologists , along with social workers , psychologists , and physical therapists . ’

More... Cardiovascular System

📖 Prevalence of cardiovascular symptoms in post-acute COVID-19 syndrome: a meta-analysis

Thu, 06 Feb 2025 17:53:51 GMT

‘The proportions of PACS [PASC/Long Covid] patients experiencing chest pain, palpitation, and hypertension as sequelae were 22%, 18%, and 19% respectively.’

�� (6 Feb 2025 ~ BMC Medicine) ‘ Prevalence of cardiovascular symptoms in post-acute COVID-19 syndrome: a meta-analysis ’.

❦ Study ~ ‘Prevalence of cardiovascular symptoms in post-acute COVID-19 syndrome: a meta-analysis’

By Huang & Li et al / BMC Medicine ( 6 Feb 2025 )

❦ Background

❦ ‘During the acute phase [ of SARS-CoV-2 infection ] , the virus induces immune hyperactivity and multi-organ damage , primarily manifesting as respiratory failure, headache, myalgia * , anosmia * ageusia * , and vascular inflammation * .

Myalgia = Muscle pain.

Anosmia = Loss of smell.

Ageusia = Loss of taste.

Vascular inflammation = Swelling and irritation of the blood vessels.

Although extensive research has been conducted on the diagnosis, pathogenesis, and acute complications of COVID-19, the long-term sequelae have emerged as an increasingly significant public health concern in the post-pandemic [ post-emergency phase ] era.

Reports of post-acute COVID-19 syndrome (PACS) [PASC/‘Long Covid’] have notably increased , with millions of individuals worldwide affected by its long-term effects.

Common symptoms include fatigue , sleep disturbances , neurological impairments , and more than 200 other manifestations .

The mechanisms underlying PACS are associated with viral replication , residual viral components causing immune dysregulation , and interactions between the host microbiome and the virus, which may lead to aberrant immune responses .

Cardiovascular disease ( CVD ) is a leading cause of global mortality, influenced by various environmental, behavioral, and metabolic factors.

Research indicates that CVD may be a significant component of PACS, although the mechanisms underlying long-term cardiac damage after COVID-19 remain poorly understood.

Two main hypotheses have been proposed:

✺ 1. A persistent viral reservoir in cardiac tissue may trigger a chronic inflammatory response following acute infection. The virus binds to its key receptor , ACE2 [angiotensin-converting enzyme 2] , leading to ACE2 downregulation , which in turn causes the accumulation of angiotensin II (Ang II), promoting endothelial inflammation , oxidative stress , and apoptosis , thus exacerbating endothelial dysfunction .

✺ 2. In later stages of infection, an autoimmune response against cardiac antigens may develop. Studies have shown an increased frequency of cardiac-specific antibodies in COVID-19 patients.

❦ The study

A systematic search of PubMed, Embase, and the Cochrane Library was conducted up to March 17, 2024 .

The primary outcomes included hypertension , palpitations , and chest pain , with pooled effect estimate reported as proportions and odds ratios ( ORs ) with 95% confidence intervals ( CIs ). Sensitivity and sub-group analysis were performed to assess the robustness of the results and to identify sources of heterogeneity.

A total of 37 studies , encompassing 2,965,467 patients , were included in the analysis.

➲ Pooled results from case-control studies revealed that, compared to the control group, the ORs [ O dds R atios ] of chest pain in the COVID-19 group was 4.0 .

➲ The ORs for palpitation and hypertension were 3.4 and 1.7 , respectively.

➲ The proportions of PACS patients experiencing chest pain , palpitation , and hypertension as sequelae were 22% , 18% , and 19% respectively.

➲ Our findings indicate that 15% of COVID-19 patients experience cardiovascular sequelae .

‘Furthermore, COVID-19 infection significantly increases the likelihood of developing these sequelae compared to uninfected individuals.’

Future research should prioritize investigating the underlying pathological mechanisms and developing targeted preventive and management strategies .’

❂

�� (6 Feb 2025 ~ BMC Medicine) Prevalence of cardiovascular symptoms in post-acute COVID-19 syndrome: a meta-analysis ➤

‘Prevalence of cardiovascular symptoms in post-acute COVID-19 syndrome: a meta-analysis.’

❦ Further reading: The heart and the cardiovascular system

�� (25 Feb 2025 ~ C19.Life) ‘ This beating heart... 70 studies and articles on SARS-CoV-2 and the cardiovascular system (2020–2024) ➤ ’.

‘ The narrative that COVID-19 had only respiratory sequelae led to a delayed realization of the neurological , cardiovascular and other multi-system impacts of COVID-19. ’

( Nature Reviews Microbiology • Jan 2023) ➲

“I would argue that COVID-19 is not a disease of the lungs at all.

It seems most likely that it is what we call a vascular and neurologic infection , affecting both nerve endings and our cardiovascular system.”

( American Heart Association • Jan 2024) ➲

More... Cardiovascular system

On the ill-fated ‘natural immunity via infection’ pipe-dream: 📖 Effectiveness of previous infection against reinfection (Omicron)

Wed, 05 Feb 2025 12:06:23 GMT

‘Before Omicron, natural infection provided strong and durable protection against reinfection, with minimal waning over time.

However, during the Omicron era, protection was robust only for those recently infected, declining rapidly over time and diminishing within a year.’

Legend: ‘ Effectiveness of previous infection against reinfection (Omicron) . ’ ➤

�� (5 Feb 2025 ~ Nature) ‘ Differential protection against SARS-CoV-2 reinfection pre- and post-Omicron ’.

❦ Study ~ ‘Differential protection against SARS-CoV-2 reinfection pre- and post-Omicron’

By Chemaitelly et al / Nature ( 5 Feb 2025 )

❦ ‘The severe acute respiratory syndrome coronavirus 2 ( SARS-CoV-2 ) has rapidly evolved over short timescales , leading to the emergence of more transmissible variants such as Alpha and Delta.

‘The arrival of the Omicron variant marked a major shift , introducing numerous extra mutations in the spike gene compared with earlier variants.

These evolutionary changes have raised concerns regarding their potential impact on immune evasion , disease severity and the effectiveness of vaccines and treatments .’

In this epidemiological study, we identified two distinct patterns in the protective effect of natural infection against reinfection in the Omicron versus pre-Omicron eras.

‘ Before Omicron , natural infection provided strong and durable protection against reinfection , with minimal waning over time.

However, during the Omicron era, protection was robust only for those recently infected , declining rapidly over time and diminishing within a year .’

These results demonstrate that SARS-CoV-2 immune protection is shaped by a dynamic interaction between host immunity and viral evolution, leading to contrasting reinfection patterns before and after Omicron’s first wave.

This shift in patterns suggests a change in evolutionary pressures, with intrinsic transmissibility driving adaptation pre-Omicron and immune escape becoming dominant post-Omicron , underscoring the need for periodic vaccine updates to sustain immunity .’

❂

�� (5 Feb 2025 ~ Nature) ‘ Differential protection against SARS-CoV-2 reinfection pre- and post-Omicron ’.

�� (5 Feb 2025 ~ Nature) Differential protection against SARS-CoV-2 reinfection pre- and post-Omicron ➤

❦ Further reading on SARS-CoV-2 genome evolution

❦ Accessed: 21 January 2024 .

➲ Genomic epidemiology of SARS-CoV-2 since pandemic start .

‘ If you are letting yourself get infected and taking no precautions against passing it on, you are not a passive bystander for your next infection.

You’ve participated in creating it. ’

❦ Accessed: 29 October 2024 .

➲ Genomic epidemiology of SARS-CoV-2 since pandemic start.

❦ Accessed: 7 September 2025 .

➲ Genomic epidemiology of SARS-CoV-2 since pandemic start .

❦ By Date .

➲ Accessed: 7 September 2025 .

➲ Genomic epidemiology of SARS-CoV-2 since pandemic start .

[ Current ➲ ]

✾

❦ More reading : On Reinfections

‘ After adjusting for relevant demographic, lifestyle, and clinical variables, we found a significant association between the risk of experiencing PASC and multiple SARS-COV-2 infections, severe COVID-19, and being unvaccinated at first infection. ’

�� (10 Oct 2024 ~ The Lancet: Regional Health ~ Western Pacific) Long COVID facts and findings: a large-scale online survey in 74,075 Chinese participants ➤

‘ Our research found that while acute symptoms of reinfection are generally milder, the severity and incidence rate of long COVID increase significantly with the number of reinfections. ’

�� (27 Mar 2024 ~ BMC Infectious Diseases) The symptoms and interval of Omicron SARS-CoV-2 reinfection among healthcare workers in a hospital of Southern China: a cross-sectional study ➤

‘ The main symptoms during the first infection in this Omicron wave were fever and sore throat, while sore throat was the main symptom in the reinfection; the average interval for SARS-CoV-2 reinfection was 149.91 days.

The reasons for COVID-19 reinfection are multifaceted, primarily including low antibody levels, the shortened duration of immune protection provided by antibodies, the mutation of viral strains, non-adherence to epidemic prevention measures by the population, hesitancy towards vaccination, and public fatigue due to the prolonged pandemic. ’

�� (22 Feb 2024 ~ Science) Solving the puzzle of Long Covid ➲

‘ Reinfection, which is now the dominant type of SARS-CoV-2 infection, is not inconsequential; it can trigger de novo Long Covid or exacerbate its severity.

Each reinfection contributes additional risk of Long Covid: cumulatively, two infections yield a higher risk of Long Covid than one infection, and three infections yield a higher risk than two infections. ’

�� (17 Feb 2024 ~ The Lancet: eClinical Medicine) Long-term risks of respiratory diseases in patients infected with SARS-CoV-2: a longitudinal, population-based cohort study ➲

‘ Our study showed a significant increase of the long-term risk of developing asthma, COPD [ Chronic Obstructive Pulmonary Disease ] , ILD [ Interstitial Lung Disease ] , and lung cancer diseases among individuals who suffered SARS-CoV-2 reinfection. ’

‘ During the SARS-CoV-2 Omicron era, reinfection patients were observed to have an increased risk of all-cause mortality. ’

�� (2 Feb 2024 ~ Nature: Communications) Risk of SARS-CoV-2 reinfection during multiple Omicron variant waves in the UK general population ➤

‘ Estimated protection against Omicron reinfections decreased over time from the most recent infection.

Those 14–180 days after receiving their most recent vaccination had a lower risk of reinfection than those >180 days from their most recent vaccination. ’

�� (8 Dec 2023 ~ Statistics Canada / Statistique Canada) Experiences of Canadians with long-term symptoms following COVID-19 ➤

‘ As of June 2023, about 2 in 3 Canadians reported at least one infection, with 1 in 5 having been infected multiple times. ’

�� (10 Nov 2022 ~ Nature: Medicine) Acute and post-acute sequelae associated with SARS-CoV-2 reinfection ➤

‘ Reinfection further increases risks of death, hospitalization and sequelae in multiple organ systems in the acute and postacute phase. ’

�� (25 May 2022 ~ Nature: Medicine) Long COVID after breakthrough SARS-CoV-2 infection ➤

‘ Vaccination before infection confers only partial protection in the post-acute phase of the disease. ’

✾

❦ On waning vaccines vs. Omicron

�� (27 Feb 2025 ~ CDC) Interim Estimates of 2024–2025 COVID-19 Vaccine Effectiveness Among Adults Aged ≥18 Years — VISION and IVY Networks, September 2024–January 2025 ➤

‘ Vaccine effectiveness (VE) of 2024–2025 COVID-19 vaccine was 33% against COVID-19–associated emergency department (ED) or urgent care (UC) visits among adults aged ≥18 years and 45%–46% against hospitalizations among immunocompetent adults aged ≥65 years, compared with not receiving a 2024–2025 vaccine dose.

VE against hospitalizations in immunocompromised adults aged ≥65 years was 40% . ’

‘ Vaccine effectiveness against SARS-CoV-2 infection declines markedly with time and Omicron variants . ’

‘ Omicron BA.2.86 and its descendants , including JN.1 (referred to as ‘JN lineages’), emerged in late 2023 and exhibited substantial divergence from co-circulating [ Omicron ] XBB lineages.

Vaccine effectiveness in the first 7–89 days after receipt of an updated [2023–2024 monovalent XBB.1.5 vaccine] dose was 54.2% against XBB lineage hospitalization , and 32.7% against JN lineage hospitalization . ’

�� (1 Aug 2024 ~ JAMA Internal Medicine) Estimated Effectiveness of the BNT162b2 XBB Vaccine Against COVID-19 ➤

‘ Effectiveness ... of the [ Pfizer ] BNT162b2 XBB vaccine was 62% against COVID-19 hospitalization , and 58% for ED or UC visits.

Older versions of COVID-19 vaccines offered little , if any , long-term protection, including against hospital admission, regardless of the number or type of prior doses received. ’

Nb. Conflict of Interest Disclosures :

“No other disclosures were reported.”

Well, thank goodness for that.

Maybe that’s why they had to end the piece with ‘...the BNT162b2 XBB vaccine provided statistically significant additional protection against a range of COVID-19 outcomes.’

Like what – having an itchy earlobe?

If 60:40 is significant protection against an ER visit or hospital admission , I’d hate to see the odds for insignificant protection.

�� (29 May 2024 ~ The New England Journal of Medicine) Durability of XBB.1.5 Vaccines against Omicron Subvariants ➤

‘ The [ XBB.1.5 ] vaccine effectiveness against infection reached a level of 52.2% after 4 weeks . It decreased to 32.6% after 10 weeks and to 20.4% after 20 weeks .

The effectiveness against hospitalization reached a level of 66.8% after 4 weeks , and decreased to 57.1% after 10 weeks .

The XBB.1.5 vaccines were less protective against JN.1 than against XBB sublineages. ’

✾

More ... Variants, Immunity and Vaccines

More ... Reinfections

❂

📖 Does COVID increase the risk of Alzheimer’s disease?

Sun, 02 Feb 2025 14:52:51 GMT

‘Scientists discover that even mild COVID-19 can alter brain proteins linked to Alzheimer’s disease, potentially increasing dementia risk.

COVID-19-positive individuals exhibited lower cognitive test performance compared to controls – equivalent to almost two years of age-related cognitive decline. ’

�� (2 Feb 2025 ~ News Medical Life Sciences) ‘Does COVID increase the risk of Alzheimer’s disease?’

‘Participants who had mild or asymptomatic COVID-19 showed alterations in their plasma biomarkers, suggesting that the infection’s impact on brain health may not be limited to severe cases.’

❦ Scientific Media Article ~ ‘ Does COVID increase the risk of Alzheimer’s disease? ’

By Dr. Chinta Sidharthan / News Medical Life Sciences ( 2 Feb 2025 )

‘A recent study published in the journal Nature Medicine investigated whether both mild and severe cases of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection are linked to changes in brain biomarkers associated with Alzheimer’s disease.

By analyzing blood samples from the United Kingdom (U.K.) Biobank participants, the researchers found that individuals who had COVID-19 showed signs of increased brain pathology, raising critical public health concerns.

Alzheimer’s disease is associated with changes in brain proteins such as beta-amyloid and tau , which can be detected in blood samples years before disease symptoms appear.

However, previous studies have focused mainly on severe COVID-19 cases , leaving a gap in understanding the risks for those with mild-to-moderate infections .

Given the emerging evidence that even mild or moderate cases of COVID-19 can result in P ost- A cute S equelae of C OVID-19 ( PASC ), this study aimed to determine whether SARS-CoV-2 infection – regardless of severity – could contribute to changes in these critical biomarkers.

‘The study found that individuals who had COVID-19 exhibited significant changes in brain biomarkers associated with Alzheimer’s disease .’

The Aβ42:Aβ40 ratio , a key marker of beta-amyloid build-up , was lower in COVID-19-positive participants compared to their matched controls. A reduced ratio of these proteins is commonly linked to Alzheimer’s pathology .

Additionally, the study observed increased levels of pTau-181 , a protein associated with tau tangles in the brain, and elevated NfL levels, which indicated neuronal damage . GFAP , a marker of astrocyte activation and neuroinflammation , was also higher in those who had COVID-19.

‘Strikingly, these biomarker changes were comparable to four years of aging or 60% of the effect size of inheriting a single APOE-ε4 allele, a well-known genetic risk factor for Alzheimer’s disease .’

These biomarker changes were more pronounced in older individuals ( particularly those over 70 years old ) and those with pre-existing risk factors such as hypertension and obesity .

‘Interestingly, even participants who had mild or asymptomatic COVID-19 showed alterations in their plasma biomarkers, suggesting that the infection’s impact on brain health may not be limited to severe cases.

The researchers also analyzed cognitive test scores and neuroimaging data , finding that COVID-19-positive individuals exhibited lower cognitive test performance compared to controls – equivalent to almost two years of age-related cognitive decline .’

Brain imaging revealed structural patterns associated with Alzheimer’s disease in some participants, further reinforcing the potential link between COVID-19 and neurodegeneration.

Additionally, the study found that certain inflammatory markers , including TNFSF10 (TRAIL), PTX3, and IL-6, were altered in post-COVID individuals, suggesting a prolonged inflammatory response that could contribute to brain pathology.

The researchers explained that while this study does not establish a direct causal link between COVID-19 and Alzheimer’s, the results raise concerns about the potential long-term neurological consequences of the viral infection.

The findings also highlighted the importance of monitoring brain health in post-COVID-19 patients and considering preventive strategies for at-risk patients .

‘Overall, the study provided new evidence that COVID-19 may accelerate Alzheimer’s disease-related brain changes , even in individuals with mild infections.’

The observed alterations in plasma biomarkers suggested a potential long-term impact on brain health .

‘While further research is needed to confirm these findings, the authors emphasized that their results align with previous reports suggesting an increased incidence of dementia following COVID-19 .’

These findings highlight the importance of long-term monitoring, preventive interventions, and future public health strategies aimed at mitigating post-COVID neurological risks.’

�� (2 Feb 2025 ~ News Medical Life Sciences) ‘Does COVID increase the risk of Alzheimer’s disease’

�� (2 Feb 2025 ~ News Medical Life Sciences) Does COVID increase the risk of Alzheimer’s disease? ➤

❂

�� (30 Jan 2025 ~ Nature Medicine) ‘Plasma proteomic evidence for increased β-amyloid pathology after SARS-CoV-2 infection’ .

❦ Study ~ ‘ Plasma proteomic evidence for increased β-amyloid pathology after SARS-CoV-2 infection ’

By Duff et al / Nature Medicine ( 30 Jan 2025 )

‘In conclusion, our study found plasma biomarker changes related to higher brain β-amyloid pathology in association with enhanced brain imaging signatures of Alzheimer’s Disease (AD) after SARS-CoV-2 infection.

While the study does not establish a causal link between infection and AD, along with earlier studies suggesting increased rates of dementia diagnosis following COVID-19, it suggests that the incidence of AD could increase following the COVID-19 pandemic.

Importantly, the relationships described here may not be specific for SARS-CoV-2 and reflect more general effects of infections on the aging brain.

Prevention of SARS-CoV-2 infection (and other systemic infections) therefore should be considered in developing risk factor modification strategies for AD in later life.’

�� (30 Jan 2025 ~ Nature Medicine) Plasma proteomic evidence for increased β-amyloid pathology after SARS-CoV-2 infection ➤

❂

❦ Related reading

�� (15 Dec 2024 ~ BMC Geriatrics) Association between COVID-19 infection and new-onset dementia in older adults: a systematic review and meta-analysis ➤

�� (3 Dec 2024 ~ eNeurologicalSci) Impact of COVID-19 on functional, cognitive, neuropsychiatric, and health-related outcomes in patients with dementia: A systematic review ➤

�� (3 Mar 2025 ~ Age Ageing) Risk of new-onset dementia following COVID-19 infection: a systematic review and meta-analysis ➤

�� (29 Jun 2023 ~ Nature Cell Death Discovery: Review Article) Long-term effects of SARS-CoV-2 infection on human brain and memory ➤

�� (Nov 2024 ~ The Lancet) Temporal association between COVID-19 infection and subsequent new-onset dementia in older adults (aged 60 years and above): a systematic review and meta-analysis ➤

�� (7 Dec 2021 ~ Alzheimer’s & Dementia Journal) Impact of COVID-19 on the Onset and Progression of Alzheimer’s Disease and Related Dementias: A Roadmap for Future Research ➤

More... Dementia

More... Brain & Nervous System

📖 Persistent symptoms and clinical findings in adults with Post-Acute Sequelae of COVID-19 / Post-COVID-19 Syndrome (PCS) in the second year after acute infection

Thu, 23 Jan 2025 17:09:47 GMT

‘The predominant symptoms, often clustering together, remain fatigue, cognitive disturbance and chest symptoms, including breathlessness, with sleep disorder and anxiety as additional complaints.

Many patients with persistent PCS [PASC/‘Long Covid’] show impaired executive functioning, reduced cognitive processing speed and reduced physical exercise capacity.’

�� (23 Jan 2025 ~ PLOS Medicine) ‘Persistent symptoms and clinical findings in adults with post-acute sequelae of COVID-19/post-COVID-19 syndrome in the second year after acute infection: A population-based, nested case-control study’.

‘The development of new symptoms related to PCS among participants initially recovered was associated with an intercurrent secondary SARS-CoV-2 infection [ COVID-19 reinfection ] .’

�� (23 Jan 2025 ~ PLOS Medicine) Figure: ‘Change in case-control status of study participants between initial questionnaire survey (Phase 1) and clinical examination (Phase 2).’

❦ Study ~ ‘ Persistent symptoms and clinical findings in adults with post-acute sequelae of COVID-19/post-COVID-19 syndrome in the second year after acute infection: A population-based, nested case-control study ’

By R.S. Peter et al / PLOS Medicine ( 23 Jan 2025 ) [Abridged]

❦ ‘We found persistence of symptoms and impairments in two-thirds of patients with PCS [ P ost- C OVID-19 S yndrome, or ‘Long Covid’] after more than 1 year following acute SARS-CoV-2 infection.

Individuals with persistent PCS [‘Long Covid’] demonstrated objective signs of cognitive deficits , and reduced exercise capacity .

Laboratory tests (including inflammatory and coagulation markers), or resting echocardiographic results, were unable to discriminate cases from controls.

These observations appear important since, unlike in many other studies, we included only adults of working age , and most study participants did not have medical treatment and were not hospitalised for their acute SARS-CoV-2 infection.

Interestingly, risk factors for non-improvement of case status in the present study included lower educational status .

‘The development of new symptoms related to PCS among participants initially recovered was associated with an intercurrent secondary SARS-CoV-2 infection [reinfection with SARS-CoV-2 ].’

Patients with persistent PCS were less frequently never smokers (61.2% versus 75.7%), [and] more often obese (30.2% versus 12.4%).

An important finding was that post-acute vaccination against SARS-CoV-2 did not appear to be associated with PCS improvement .

Fatigue and cognitive disturbance were the most prevalent health problems ( more than 60% for each cluster) among individuals with persistent PCS.

Of note were the large overlap between self-reported fatigue , cognition problems and chest symptoms , and the strong correlation of various symptom ratings with health-related quality of life scores.

‘ Extreme fatigue affected approximately one-tenth of the patients with persistent PCS [Post-COVID-19 Syndrome, or ‘Long Covid’] , while PEM [Post-Exertional Malaise] lasting more than 14 hours was reported by 36% .

Cognitive disturbance was the second most frequent symptom cluster, with concentration problems being slightly more often reported than memory problems .’

A similar observation independent of the time after acute infection has also been made in a large online survey among subjects with complaints for at least 3 months after infection [ ✪ ] .

[ ✪ ] Brus et al . The prolonged impact of COVID-19 on symptoms, health-related quality of life, fatigue and mental well-being: a cross-sectional study. Front Epidemiol. 22 Jun 2023.

In a large claims data network analysis of neurologic and psychiatric sequelae, Taquet and colleagues [ ✪ ] found that risks of cognitive deficits , dementia , psychotic disorders and epilepsy / seizures remained increased over a 2-year follow-up period after SARS-CoV-2 infection, which was unlike the risks of (other) common psychiatric disorders that rapidly returned to baseline.

[ ✪ ] Taquet et al . Neurological and psychiatric risk trajectories after SARS-CoV-2 infection: an analysis of 2-year retrospective cohort studies including 1 284 437 patients. Lancet Psychiatry. 17 Aug 2022.

Other studies also reported persisting or increasing cognition or concentration problems with generally decreasing rates of other symptoms and physical health over time [ ✪ ] .

[ ✪ ] Cheetham et al . The effects of COVID-19 on cognitive performance in a community-based cohort: a COVID symptom study biobank prospective cohort study. EClinicalMedicine. 21 Jul 2023.

[ ✪ ] Latifi A, Flegr J. Is recovery just the beginning? Persistent symptoms and health and performance deterioration in post-COVID-19, non-hospitalized university students – a cross-sectional study. Biol Methods Protoc. 6 Dec 2023.

A memory questionnaire study found worse memory problems up to 3 years after acute infection (when compared to uninfected controls) [ ✪ ] , and a recent elegant study showed reaction time slowing with increasing time after acute SARS-CoV-2 infection [ ✪✪ ] .

[ ✪ ] Ellingjord-Dale et al . Prospective memory assessment before and after Covid-19. N Engl J Med. 28 Feb 2024.

[ ✪✪ ] Zhao et al . Long COVID is associated with severe cognitive slowing: a multicentre cross-sectional study. EClinicalMedicine. 25 Jan 2024.

Taken together, these findings and the results of our study indicate that cognition problems might, in fact, tend more to chronicity than other health problems of PCS patients.

Sleep disorder , in particular insomnia , was another frequent complaint among cases. Pooled data of previous studies on more than 15,000 participants revealed a prevalence of 40%–50% for sleep disorder among individuals with PCS, which is comparable to our data.

Neurocognitive testing showed significant group differences, indicating cognition deficits concerning attention and executive functioning , with problems in divided attention and lower processing speed in patients with persistent PCS , and this finding appeared to be independent of pre-existing illnesses.

Impaired executive functioning and reduced processing speed , as observed here in persistent PCS, is in agreement with a report of similar deficits in a large registry cohort [ ✪ ] of COVID-19 patients, with pronounced cognitive slowing in 270 patients from two PCS cohorts [ ✪✪ ] , and with attention and executive function deficits in a comprehensive cognitive assessment of patients with PCS after mostly mild initial disease [ ✪✪✪ ] .

[ ✪ ] Becker et al . Assessment of cognitive function in patients after COVID-19 infection. JAMA Netw Open. 22 Oct 2021.

[ ✪✪ ] Zhao et al . Long COVID is associated with severe cognitive slowing: a multicentre cross-sectional study. EClinicalMedicine. 25 Jan 2024.

[ ✪✪✪ ] Delgado-Alonso et al . Cognitive dysfunction associated with COVID-19: a comprehensive neuropsychological study. J Psychiatr Res. 26 Mar 2022.

An impaired physical exercise capacity with reduced handgrip strength (or 6-min walk test ) and reduced VO₂ max * appear to be hallmark signs of PCS.

* VO₂ max : Maximum rate of oxygen consumption as measured during incremental exercise, most typically on a motorised treadmill.

One of the strengths of the present study is the nested, population-based approach in defined geographic regions with a large number of individuals with PCR-confirmed earlier infection , regardless of the need for medical treatment .

We focussed on adults in the working age-group .

We avoided an over-representation of hospitalised elderly patients who are likely to show more SARS-CoV-2-non-specific adverse health sequelae due to more severe acute infection, comorbidities and ageing.

As a conclusion, we report that two-thirds of patients with PCS [Post-COVID-19 Syndrome / PASC / ‘Long Covid’] 6–12 months after acute SARS-CoV-2 infection continue to report persistent symptoms interfering with daily living and associated with reduced quality of life and/or work ability .

The symptoms appear to change slightly but the predominant symptoms , often clustering together, remain fatigue , cognitive disturbance and chest symptoms , including breathlessness , with sleep disorder and anxiety as additional complaints in a substantial proportion of cases.

In a thorough medical examination, many patients with persistent PCS show findings that significantly differ from controls and are in part abnormal/out of reference; these include impaired executive functioning , reduced cognitive processing speed and reduced physical exercise capacity only in part explained by deconditioning and typically unrelated to central cardiac or pulmonary limitations.’

❂

�� (23 Jan 2025 ~ PLOS Medicine) Persistent symptoms and clinical findings in adults with post-acute sequelae of COVID-19/post-COVID-19 syndrome in the second year after acute infection: A population-based, nested case-control study ➤

❂

More... Post-Exertional Malaise (PEM)

More... PCS (PASC / ‘Long Covid’)

On the 700-day cough

Sat, 16 Nov 2024 10:29:29 GMT

❦ On that 700-day cough...

It’s a new thing, but it’s only reserved for inside supermarkets and offices. And pharmacies and hospitals and care homes.

Oh, and your living-room.

But apart from that, it’s not exactly a deal-breaker.

I mean, c’mon. They put up with way worse in the 1900s.

More... On the Respiratory System

More by... C19.Life

On volunteering for infection, and spinning the evolutionary wheel

Tue, 29 Oct 2024 16:35:13 GMT

❦ “If you are letting yourself get infected and taking no precautions against passing it on, you are not a passive bystander for your next infection.

You’ve participated in creating it.”

❦ Genomic epidemiology of SARS-CoV-2 since pandemic start.

➲ Data accessed: 21 Jan 2024 .

❦ Genomic epidemiology of SARS-CoV-2 since pandemic start.

➲ Data accessed: 29 Oct 2024 .

❦ Genomic epidemiology of SARS-CoV-2 since pandemic start.

➲ Data accessed: 29 Sep 2025 .

✾ See current : ⚒ C-19 Resource: Genomic Mapping of SARS-CoV-2 / COVID-19 Variants ➲

✾

More... ⚒ Resources

📖 Clinical and functional assessment of SARS-CoV-2 sequelae among young marines – a panel study

Wed, 23 Oct 2024 12:11:45 GMT

❦ ‘In this population of healthy young adult US Marines with mostly either asymptomatic or mild acute COVID-19, one fourth reported physical , cognitive , or psychiatric long-term sequelae of infection.

The Marines affected with PASC [Post-Acute Sequelae of COVID-19 / Post-COVID-19 Complications / ‘Long Covid’] showed evidence of long-term decrease in functional performance suggesting that SARS-CoV-2 infection may negatively affect health for a significant proportion of young adults .’

❂

‘Among the 899 participants, 88.8% had a SARS-CoV-2 infection.

Almost a quarter (24.7%) of these individuals had at least one COVID-19 symptom that lasted for at least 4 weeks meeting the a priori definition of PASC established for this study.

Among those with PASC, 10 had no acute SARS-CoV-2 symptoms after PCR-confirmed infection suggesting that PASC can occur among asymptomatic individuals.

Many participants reported that lingering symptoms impaired their productivity at work, caused them to miss work, and/or limited their ability to perform normal duty/activities.

Marines with PASC had significantly decreased physical fitness test scores up to approximately one year post-infection with a three-mile run time that averaged in the 65th percentile of the reference cohort.

[ PASC was associated with a significantly increased 3-mile run time on the standard Marine fitness test. PASC participants ran 25.1 seconds slower than a pre-pandemic reference cohort composed of 22,612 Marine recruits from 2016 to 2019.

A three-mile run evaluates aerobic exercise , overhead lifting of an ammunition can and pull-ups evaluate strength , and shooting a rifle evaluates fine-motor skills .]

Scores for events evaluating upper body (pull-ups, crunches, and ammo-can lift) were not significantly reduced by PASC; however, overall physical fitness scores were reduced.

‘The poorer run times and overall scores among PASC participants are indicative of on-going functional effects.’

Standardized health-based assessments for somatization, depression, and anxiety further highlighted the detrimental health effects of PASC.

Almost 10% of participants with PASC had PHQ-8 scores ≥10. Increased somatization * has been associated with increased stress, depression, and problems with emotions.

* [ Somatization / Somatisation = Medical symptoms caused by psychological stress.]

Additionally, PASC participants had higher GAD-7 scores suggesting increased anxiety in a population with unique inherent occupational stressors associated with higher rates of anxiety, depression, and post-traumatic stress disorder.

‘Increased severity of anxiety among those with PASC, combined with greater rates of mental health disorders in general, could portend an ominous combination and should be closely followed.’

Like others, we identified cardiopulmonary symptoms as some of the most prevalent.

The high prevalence of symptoms like shortness of breath, difficulty breathing, cough, and fatigue is particularly notable when combined with decreased objective measures of aerobic performance such as running.

These results suggest pathology in the cardiopulmonary system.

In contrast we observed no reduction in scores assessing strength and marksmanship suggesting the lack of detectable pathology in the neuro-musculoskeletal system.

We have previously found in this same cohort that SARS-CoV-2 infection causes prolonged dysregulation of immune cell epigenetic patterns like auto-immune diseases.

Based on the reported PASC symptoms, the potential current and future public health implications in this population could be substantial.

‘Chronic health complications from PASC, especially in a young and previously healthy population with a long life expectancy, could decrease work productivity and increase healthcare costs.’

Significant changes in the Years-of-Life lived with a disability can disproportionally increase disability-adjusted life-years, and should be considered when allocating resources and designing policy.’

❂

�� (23 Oct 2024 ~ The Lancet: Regional Health/America) Clinical and functional assessment of SARS-CoV-2 sequelae among young marines – a panel study ➤

➲ ' Clinical and functional assessment of SARS-CoV-2 sequelae among young marines – a panel study', by Porter et al .

➲ Date accessed: 8 Nov 2024 .

On flattening the curve

Sun, 20 Oct 2024 09:06:10 GMT

❦ If parents, and politicians and teachers, and healthcare workers and public health bodies wanted things to change, all they need do is read .

It’s all there.

But they don’t. They won’t.

And they insist on their medical and scientific flat-earthing – hand-sanitiser for aerosol-transmitted disease – because they prefer the world to be flat.

So let them walk off the edge of the world.

[ Caveat: The earth is not flat, and doing nothing will not flatten the curve – but walk far enough, and you are likely to fall off a cliff.]

✾

Read... or walk...

📖 Post-COVID-19 syndrome among 5248 healthcare workers in England: Longitudinal findings from NHS CHECK

Tue, 08 Oct 2024 12:09:48 GMT

‘This study included 5248 healthcare workers. While 33.6% reported prolonged COVID-19 symptoms consistent with PCS, only 7.4% reported a formal diagnosis of PCS.

Fatigue, difficulty concentrating, insomnia, and anxiety or depression were the most common PCS [Post-COVID-19 Syndrome] symptoms.

Baseline risk factors for reporting PCS included screening for common mental disorders, direct contact with COVID-19 patients, pre-existing respiratory illnesses, female sex and older age.’

✾

‘ Post-COVID-19 syndrome among 5248 healthcare workers in England: longitudinal findings from NHS CHECK .’

❦ Post-COVID-19 syndrome among 5248 healthcare workers in England: Longitudinal findings from NHS CHECK

By Dempsey et al / BMJ Journals ~ Occupational & Environmental Medicine ( 8 Oct 2024 )

Abstract

‘The objectives of this study were to examine Post-COVID-19 syndrome (PCS) [ PASC / ‘Long Covid’ ] among healthcare workers (HCWs) in England and explore risk factors for the condition.’

Methods

‘Data were collected by National Health Service (NHS) CHECK, a longitudinal study exploring HCWs’ mental and physical well-being during and after the [ emergency phase of the ] COVID-19 pandemic.

NHS CHECK collected data at four timepoints: the baseline survey between April 2020 and January 2021, and then three follow-up surveys at approximately 6, 12 and 32 months post baseline. PCS data were collected at 12 and 32 months, while risk factor data were from baseline.

HCWs were asked what COVID-19 symptoms they experienced and for how long and were classified as having PCS if they had any symptom for ≥12 weeks. Multi-level regressions were used to examine risk factors for PCS.’

Results

‘This study included 5248 HCWs . While 33.6% reported prolonged COVID-19 symptoms consistent with PCS, only 7.4% reported a formal diagnosis of PCS.’

‘ Fatigue , difficulty concentrating , insomnia and anxiety or depression were the most common PCS symptoms .

Baseline risk factors for reporting PCS included screening for common mental disorders , direct contact with COVID-19 patients , pre-existing respiratory illnesses , female sex and older age .’

Conclusions

‘While a third of HCWs reported prolonged COVID-19 symptoms consistent with PCS, a smaller percentage reported a formal diagnosis of the condition.

We replicate findings that direct contact with COVID-19 patients, older age, female sex, pre-existing respiratory illness and symptoms of common mental disorders are associated with increased risk of PCS.’

Notes

‘Healthcare workers (HCWs) were [ sic ] at high risk to COVID-19 infection.

In the UK, research using data from the ONS COVID-19 Infection Survey found that HCWs were at higher risk of contracting COVID-19 compared with non-essential workers, though this effect reversed by June 2021.

Another study found that HCWs were among the occupational groups to self-report higher prevalences of COVID-19 symptoms lasting 4 or more weeks.

ONS mortality data revealed that those working in the healthcare sector were more likely to die of COVID-19 in 2020 compared with other industries, with this effect diminishing thereafter.

‘Given the increased risk of COVID-19 infection among HCWs , particularly early in the pandemic, they are likely to be at high risk of PCS .

This may also be the case for other essential workers , with educators , bus and coach drivers , and police and protective services staff also at increased risk .’

Due to the associated symptoms and lack of a known mechanism, PCS has drawn comparisons with other conditions, such as myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS).

ME/CFS is a long-term condition defined by post-exertional malaise , which may have a delayed onset, physical and mental fatigue and fatigability, issues with sleeping, memory or concentration, and functional impairment, which may be substantial.

Diagnoses are made if the defining symptoms last for 6 months or longer and cannot be attributed to an alternative cause.’

Risk factors for PCS

‘We found a very strong association between meeting the GHQ-12 cut-off score at baseline, indicating probable CMDs , and reporting PCS symptoms at follow-up.

Having direct contact with COVID-19 patients also had a very strong association with reporting PCS symptoms, while having asthma / COPD or female sex had a strong association .

Associations were also observed for age, as those aged between 51 and 60 were more likely to report PCS, and job role, where doctors were less likely to report PCS.’

‘Associations were also observed for age , as those aged between 51 and 60 were more likely to report PCS , and job role , where doctors were less likely to report PCS .’

✾

�� (8 Oct 2024 ~ BMJ Journals: Occupational & Environmental Medicine) Post-COVID-19 syndrome among 5248 healthcare workers in England: Longitudinal findings from NHS CHECK ➤

✾

More... On Healthcare Workers

More... Healthcare Worker insights

On Dying of Whatever

Sun, 26 May 2024 17:52:55 GMT

❦ NHS nurse in 1990:

— “Shit, I just got a needlestick injury.”

❦ 2024:

— “Yeah, well, whatever. We all gotta die of something.”

✾

More C-19 Cartoons ➲

More by... C19.Life

✒ In History: ‘The Ventilation and Warming of School Buildings’ (1887)

Wed, 10 Apr 2024 21:25:39 GMT

‘In those school-rooms where ventilation is imperfect and the air impure, six sevenths of the money expended to educate a child is wasted.’

❂

The Ventilation and Warming of School Buildings (1887)

By Gilbert B. Morrison

Published by D. Appleton and Company, New York. 1887.

Accessed 10 Apr 2024

Preface (p.xxii)

❦ ‘I am fully convinced that people are prematurely dying by thousands simply from a lack of correct and positive convictions concerning impure air; for, when the true nature of a danger is fully appreciated, the requisite means to avert it will generally be found.’

❂

Chapter II: The Effects Of Breathing Impure Air (pp.20-23)

❦ ‘Impure air is also believed by the best authorities to be one of the principal causes of epidemics. Dr. Carpenter, than whom there is no abler authority, says:

“It is impossible for anyone who carefully examines the evidence to hesitate for a moment in the conclusion that the fatality of epidemics is almost invariably in precise proportion to the degree in which an impure atmosphere has been habitually respired.”

The Board of Health of New York conclude that forty per cent of all deaths are caused by breathing impure air.

In view of such alarming facts, this same board declares:

“Viewing the causes of preventable diseases, and their fatal results, we unhesitatingly state that the first sanitary want in New York and Brooklyn is ventilation .”

Direct experiment proves that the air in our school-rooms is impure in almost all cases, and in a majority of them to a degree far beyond the danger line.

In view of these facts, and the results as proved by the authorities above cited, why is it regarded by the public with such indifference?

When a school-house is blown down by a hurricane, killing and maiming a score of children, it is justly regarded as a great calamity; a vacation is given to quiet the excited fears of parents and children; investigating committees are appointed to locate the responsibility, and the faces of the whole populace are blanched with apprehension.

Why is this?

Why does the intelligent parent send his child to a school-room poorly ventilated and crowded with children, some of whom are breathing into a stagnant air the germs of disease and death, while others, from unwashed bodies, are delivering into it their deadly emanations, and all without a protest on the part of those even who provide proper hygienic conditions at home?

It is because the effects of the one are immediate, occupy little time, the number killed can be actually counted, and the exact magnitude of the calamity estimated all at once.

In the other case the process is slower, but of far greater extent; the actual results are by the general public less definitely known, and custom and attention to other matters divert the attention, and the deadly destruction of the innocents by impure air goes on silently, constantly, and powerfully.

While noisy demonstrations like that of the cyclone attract attention, and inspire fear and terror, it is in the silent forces that the danger lies.

Nature’s most destructive forces, as well as her strongest constructive ones, are silent in their operations; but when Science detects a silent, insidious enemy to human welfare, it is not only our duty to assume an attitude of self-defense and self-protection, but it should be regarded as folly not to do so.’

❦ On high CO₂ levels connected to poor performance in schools:

‘The effects of breathing impure air thus far considered are pathological, but it has its pedagogical and economical aspects. Every observing teacher knows the immediate relation between the vitiated air in the school-room and the work he wishes the pupils to perform.

Much of the disappointment of poor lessons and the tendency to disorder are due directly to this cause.

The brain unsupplied with a proper amount of pure blood [oxygen] refuses to act, and the will is powerless to arouse the flagging energies; the general feeling of discomfort, dissatisfaction, and unrest which always accompanies a bad state of the blood.

From an economical standpoint it would, of course, be impossible to estimate the financial waste of breathing impure air, but it can not but be enormous.

In any discussion of the feasibility of incurring the additional expense of the most perfect ventilation, this loss occasioned by the want of such ventilation must not be ignored.’

❂

Chapter III: The Air (pp.25-26)

❦ On ventilation, air filtration, and the super-spreading of diverse diseases in classrooms:

‘Wherever an unusual amount of unwholesome matter is being evolved, there especially should the purifying conditions be present; air in such places, to remain pure, must be changed in rapid succession, in order that dilution, diffusion, and oxidation may fulfill their legitimate functions.

In a school-room the contaminating process can not but be rapid, and wherever ample provision is not made for rapidly changing the air of the room a dangerous condition of affairs is sure to exist.

Bacteria of many forms, and spores of fungi, are also found in the air, and all these organisms are known to thrive in the organic impurities found in the air.’

❂

Chapter IV: Examination Of The Air (p.33)

❦ On measuring CO₂ levels as a proxy to establishing content of (infectious) re-breathed air:

‘A complete analysis of impure air comprehends the quantitative and qualitative tests for carbonic [sic] dioxide, free ammonia, and other nitrogenous matter, oxidizable matters, nitrous and nitric acids, and hydrogen sulphide; but for ordinary practical purposes the determination of the CO₂ is by far the most important, and is ordinarily the only one which need be made.

While the poisonous qualities of the air are not wholly due to the presence of the CO₂ per se, the amount of this gas found to be present is, in air made impure by respiration, generally a good measure for other impurities to which the poisonous quality is principally due.

Owing to this fact, a careful test for the amount of CO₂ contained in a given atmosphere is generally the only one which need be made where air is tested merely to determine its respiratory purity.’

❂

�� (Accessed 10 Apr 2024 ~ D. Appleton & Company / Google Books) The Ventilation and Warming of School Buildings ➤

❂

My thanks to Maarten De Cock for alerting me to this gem of a book. ➲

�� (Accessed 10 Apr 2024 ~ D. Appleton & Company / Google Books) The Ventilation and Warming of School Buildings by Gilbert D. Morrison ➤

‘Every person exhales carbon dioxide (CO₂).

SARS-CoV-2-positive people exhale airborne virus particles at the same time. While we cannot detect virus particles in the air , we can detect CO₂ .

This means measured indoor CO₂ levels can serve as a proxy , or an approximation, of the quantity of virus in the air that you are breathing.

As the measured CO₂ levels in an enclosed space increase, you are breathing more air that has been in other people’s lungs.

This is referred to as “re-breathed” air.

An increase in re-breathed air increases the risk of exposure to (and transmission of) SARS-CoV-2 – not to mention cognitive impairment (at 1,000+ ppm), and cognitive dysfunction (>2,500+ ppm).’

❦ Carbon dioxide (CO₂) monitor with app

The industry-standard CO₂ monitor: the Aranet4 Home. Unbiased review by HouseFresh.com ➤ .

Aranet4 Home at Amazon.co.uk.

Custom decal by Amanda Hu .

❦ Further reading on schools, transmission, children, and clean air

❦ SARS-CoV-2 – the virus that causes Covid-19 – is airborne.

➲ On airborne transmission of Covid-19 (2024) ➤

❂

❦ ‘There is robust evidence supporting the airborne transmission of many respiratory viruses, including measles virus, influenza virus, respiratory syncytial virus ( RSV ), human rhinovirus (hRV), adenovirus , enterovirus , severe acute respiratory syndrome coronavirus ( SARS [-CoV-1]) , Middle East respiratory syndrome coronavirus ( MERS -CoV), and SARS-CoV-2 .’

➲ Airborne transmission of respiratory viruses (2021) ➤

❂

❦ ‘The magnitude of the outbreak illustrates how younger children infected from diverse pediatric facilities can be a major source of widespread household transmission with the potential to facilitate community transmission in the era of the Omicron variant.’

➲ Widespread Household Transmission of SARS-CoV-2 B.1.1.529 (Omicron) Variant from Children, South Korea (2022) ➤

❂

❦ ‘Parents should not be put in a position in which they are being forced to choose between their child’s health and their child’s education.’

➲ On children, education, risk and stating the obvious (2023) ➤

❂

➲ On students, schools, supply teachers and the cost of sickness (2023) ➤

❂

❦ ‘The law imposes a responsibility on the employer to ensure safety at work for all their employees. Failure to do so could result in a criminal prosecution in the Magistrates Court or a Crown Court.

Failure to ensure safe working practices could also lead to an employee suing for personal injury or in some cases the employer being prosecuted for corporate manslaughter.’

➲ Health & Safety At Work Act (1974) ➤

❂

❦ ‘Long COVID impacts children of all ages. Fatigue, headache, dizziness, dyspnoea, chest pain, dysosmia, dysgeusia, reduced appetite, concentration difficulties, memory issues, mental exhaustion, physical exhaustion and sleep issues were between 2 and 36 times more likely in individuals with Long COVID aged 15-19 .’

➲ Long COVID in children (2023) ➤

❂

❦ “The price that children pay for being so good at getting rid of the virus in the first place is that they don’t have the opportunity to develop ‘adaptive’ memory to protect them the second time they are exposed to the virus.”

➲ Children’s immune systems do not develop ‘adaptive memory’ to protect against second-time SARS-CoV-2 infection (2023) ➤

❂

❦ ‘Death is not the main risk facing most children. Disability is. Research shows the risks of harm and disability from COVID infection are serious, and risks accumulate with additional reinfections .’

➲ Treating kids as invulnerable is treating them as disposable (2023) ➤

❂

❦ ‘The prevalence of Long COVID in children and adolescents was 25.24% .’

➲ Long COVID in children and adolescents: a systematic review and meta-analyses (2022) ➤

❂

❦ ‘Fatigue in this [adolescent] population often leads to difficulty with physical and cognitive activity, which can limit participation in school, extracurricular activities, and sports.’

➲ Long-Term COVID-19 Sequelae in Adolescents (2022) ➤

❂

❦ ‘Symptoms such as fatigue, headache, muscle and joint pain, rashes and heart palpitations and issues such as lack of concentration and short-term memory problems were particularly frequent and confirm previous observations, suggesting that they may characterize this condition.’

➲ Clinical characteristics, activity levels and mental health problems in children with long coronavirus disease: a survey of 510 children (2022) ➤

❂

❦ ‘A recent US Centers for Disease Control and Prevention (CDC) analysis of 1.4 million children aged under 12 years and 1.7 million adolescents aged 12-17 years found increased rates of asthma, myocarditis and cardiomyopathy, cardiac dysrhythmias, diabetes, renal failure, venous thromboembolism, and coagulation disorders in children with laboratory-confirmed COVID-19 compared with children without COVID-19.’

➲ Balancing the medical and social needs of children during the COVID-19 pandemic (2023) ➤

❂

❦ “I think a big problem is that many people’s conceptions of morality do not extend to invisible viral transmission and indirect chains of harm.”

➲ On invisible viral transmission, indirect chains of harm, learned negligence, and killing other people (2023) ➤

❂

➲ Comment: On choices and consequences (2023) ➤

❂

➲ Comment: On shared air and swimming pools (2024) ➤

❂

❦ Ryan Hisner pulls apart the real-life Animal Farm theatre playing out between Man, Pig and The Economy in his 2022 essay on swine, clean air, and bringing home the bacon.

➲ On pigs, clean air, and bringing home the bacon ➤

❂

➲ Elsewhere at C19.Life ~ On Transmission ➤

❂

➲ Elsewhere at C19.Life ~ On Babies and Children ➤

❂

☰ 27 studies & articles on... Airborne transmission of pathogens, and SARS-CoV-2 (COVID-19)

Mon, 04 Mar 2024 13:18:36 GMT

❦ A comprehensive collection of review articles from 1987 to 2022 regarding airborne transmission of pathogens , curated by Jonathan Mesiano-Crookston.

❂ Accessed : 4 March 2024 .

�� (November 2022 ~ Geoscience Frontiers) Aerosol Transmission of Human Pathogens: From Miasmata to Modern Viral Pandemics and Their Preservation Potential in the Anthropocene Record ➤

�� (21 Aug 2022 ~ Indoor Air) What were the historical reasons for the resistance to recognizing airborne transmission during the COVID-19 pandemic? ➤

�� (31 Jan 2022 ~ Indoor Air: Editorial) Hypothesis: All respiratory viruses (including SARS-CoV-2) are aerosol-transmitted ➤

�� (November 2021 ~ Interface Focus) How Did We Get Here: What Are Droplets and Aerosols and How Far Do They Go? A Historical Perspective on the Transmission of Respiratory Infectious Diseases➤

�� (27 Aug 2021 ~ Science ) Airborne Transmission of Respiratory Viruses ➤

�� (August 2021 ~ Nature Reviews: Microbiology) Transmissibility and Transmission of Respiratory Viruses ➤

�� (July 2021 ~ Annual Review of Biomedical Engineering) Fluid Dynamics of Respiratory Infectious Diseases ➤

�� (14 May 2021 ~ Science) A Paradigm Shift to Combat Indoor Respiratory Infection ➤

�� (1 May 2021 ~ The Lancet) Ten Scientific Reasons in Support of Airborne Transmission of SARS-CoV-2 ➤

�� (18 Jan 2021 ~ Clinical Infectious Diseases) Airborne Transmission of SARS-CoV-2: What We Know ➤

�� (12 Jan 2021 ~ The Journal of Hospital Infection) Dismantling Myths on the Airborne Transmission of Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) ➤

�� (1 Jan 2021 ~ Canadian Medical Association Journal) Mitigating Airborne Transmission of SARS-CoV-2 ➤

�� (November 2020 ~ Environment International) Aerosol Transmission of SARS-CoV-2? Evidence, Prevention and Control➤

�� (16 Oct 2020 ~ Science) Airborne Transmission of SARS-CoV-2 ➤

�� (1 Sep 2020 ~ Environment International) How Can Airborne Transmission of COVID-19 Indoors Be Minimised? ➤

�� (August 2020 ~ Anaesthesia) Airborne Transmission of Severe Acute Respiratory Syndrome Coronavirus-2 to Healthcare Workers: A Narrative Review ➤

�� (6 July 2020 ~ Clinical Infectious Diseases) It Is Time to Address Airborne Transmission of Coronavirus Disease 2019 (COVID-19) ➤

�� (June 2020 ~ Environment International) Airborne Transmission of SARS-CoV-2: The World Should Face the Reality➤

�� (May 2020 ~ Risk Analysis) Consideration of the Aerosol Transmission for COVID‐19 and Public Health➤

�� (16 April 2020 ~ The Journal of Infectious Diseases) Airborne or Droplet Precautions for Health Workers Treating Coronavirus Disease 2019? ➤

�� (26 March 2020 ~ JAMA) Turbulent Gas Clouds and Respiratory Pathogen Emissions: Potential Implications for Reducing Transmission of COVID-19 ➤

�� (28 Aug 2019 ~ Encyclopedia of Microbiology) Airborne Infectious Microorganisms ➤

�� (31 Jan 2019 ~ BMC Infectious Diseases) Recognition of Aerosol Transmission of Infectious Agents: A Commentary➤

�� (September 2016 ~ American Journal of Infection Control) Generic Aspects of the Airborne Spread of Human Pathogens Indoors and Emerging Air Decontamination Technologies ➤

�� (15 Nov 2011 ~ Advances in Preventive Medicine) Preventing Airborne Disease Transmission: Review of Methods for Ventilation Design in Health Care Facilities ➤

�� (October 2006 ~ The Journal of Hospital Infection) Factors Involved in the Aerosol Transmission of Infection and Control of Ventilation in Healthcare Premises ➤

�� (January 1987 ~ Critical Reviews in Environmental Control) Spread of Viral Infections by Aerosols➤

✾

‘Illustration of droplets and aerosols released during talking; these may carry viruses if the person is infected.

The large droplets fall rapidly to the ground in close proximity.

The small aerosols are much more concentrated in close proximity, and they can remain floating in the air and spread throughout the room, leading to (reduced) exposure at a distance.’

�� (12 Jan 2021 ~ Journal of Hospital Infection) Dismantling myths on the airborne transmission of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) ➤

Studies, articles & comment on... Airborne SARS-CoV-2 transmission

On airborne transmission of SARS-CoV-2 (COVID-19)

Wed, 28 Feb 2024 20:00:17 GMT

❦ SARS-CoV-2 – the virus that causes COVID-19 – is airborne .

In May 2021, the WHO officially recognised that SARS-CoV-2 is airborne via microscopic aerosols – meaning that the virus is transmissible through the air at both long and short range .

✾

Infographic illustrating short- and long-range airborne transmission of SARS-CoV-2 (COVID-19).

❦ Infections from direct body contact (eg. holding hands), or from fomites (touching infected objects) are low-risk .

The airborne route , via short- or long-range aerosol , is high risk and acknowledged to be the primary and dominant form of transmission.

❦ What are ‘aerosols’?

Aerosols are microscopic droplets suspended in the air, and move through a space much like cigarette smoke .

�� (29 Oct 2020 ~ El País) A room, a bar and a classroom: how the coronavirus is spread through the air ➤

‘Without air-filtration or ventilation, infectious aerosols remain suspended in the air, becoming increasingly concentrated as time goes by.’

❦ While larger droplets are commonly produced by coughing or sneezing, airborne aerosols are produced when a person exhales – including breathing , talking , singing , shouting , coughing or sneezing .

�� (29 Oct 2020 ~ El País) A room, a bar and a classroom: how the coronavirus is spread through the air ➤

‘Six people get together in a private home, one of whom is infected.

Irrespective of whether safe distances are maintained, if the six people spend four hours * together talking loudly without wearing a face mask in a room with no ventilation, five will become infected.’

* Note : The infectiousness of SARS-CoV-2 has greatly increased since this 2020 scenario: infection times with current 2025 variants can be counted in seconds and minutes than hours.

❦ And while heavier droplets fall to the ground within seconds, infectious aerosols can accumulate and stay airborne for minutes to hours in enclosed spaces .

�� (17 Jun 2020 ~ El País) An analysis of three Covid-19 outbreaks: how they happened and how they can be avoided ➤

❦ Virus-laden aerosols can be present and cause infection long after an infected person has left a room , a shop, a hospital, a GP’s surgery, a pharmacy, a classroom, a bus or a train.

�� (17 Jun 2020 ~ El País) An analysis of three Covid-19 outbreaks: how they happened and how they can be avoided ➤

❦ ‘ Buildings play a critical role in minimising , or conversely exacerbating , the spread of airborne infectious diseases .

COVID-19 outbreaks largely occur indoors – and in-room long-range transmission beyond two meters (six feet) has been well-documented in conditions with no masking and low ventilation rates.’

�� (1 Apr 2021 ~ The Lancet COVID-19 Commission) The Lancet COVID‐19 Commission Task Force on Safe Work, Safe School, and Safe Travel: Designing infectious disease resilience into school buildings through improvements to ventilation and air cleaning . ➲

“Droplets and surfaces are very convenient for people in power – all of the responsibility is on the individual.

On the other hand, if you admit [ SARS-CoV-2 ] is airborne, institutions, governments, and companies have to do something.”

Professor Jose-Luis Jimenez (2 Oct 2021) ➤

�� (29 Oct 2020 ~ El País) A room, a bar and a classroom: how the coronavirus is spread through the air ➤

‘The riskiest scenario [in a school] is a classroom with no ventilation and the teacher – Patient Zero – as the infected person.

If two hours * are spent in the classroom with an infected teacher, without taking any measures to counter the number of aerosols, there is the risk that up to 12 students could become infected.’

* Note : The infectiousness of SARS-CoV-2 has greatly increased since this early 2020 scenario: airborne person-to-person infections can be counted in seconds and minutes ( 2025 variants ) than hours.

Infected asymptomatic people (people who are infectious but not showing symptoms, or up to 60% of transmission cases ) may not be aware that they are ejecting virus-laden aerosols into the air that you breathe.

Other serious and potentially life-threatening airborne infectious diseases spread by aerosol include:

Measles
TB (tuberculosis)
Influenza
Respiratory Syncytial Virus (RSV)
Human Rhinovirus (HRV)
Pneumonia
Adenovirus
Enterovirus
Severe Acute Respiratory Syndrome Coronavirus (SARS-1)
and Middle East Respiratory Syndrome Coronavirus (MERS-CoV).

‘Our very serious concerns relate to the risk of aerosol / airborne infection ; RCN and BMA members working in all settings are raising concerns that they are not adequately protected .

Our members are concerned that fluid-repellent surgical face masks [ FRSM ] and face coverings , as currently advised in most general healthcare settings, do not protect against smaller more infective aerosols .’

The Royal College of Nursing (RCN) and The British Medical Association (BMA) ~ (21 Jan 2021) ➲

➲ Video ~ “Don’t breathe it in.”

✾ by The John Snow Project (July 2022).

More Primers at The John Snow Project) ➤

➲ Video ~ “It’s over.”

✾ by The John Snow Project (May 2022).

More Insights at The John Snow Project ➤

✾ Research-level science articles on airborne transmission and prevention at CovidisAirborne.org ➤

✾ Media articles on airborne transmission and prevention at CovidisAirborne.org ➤

Studies, articles & comment on... Airborne SARS-CoV-2 transmission

More on... Transmission

📖 Solving the puzzle of Long Covid

Thu, 22 Feb 2024 19:26:00 GMT

‘Reinfection, which is now the dominant type of SARS-CoV-2 infection, is not inconsequential; it can trigger de novo Long Covid or exacerbate its severity.

�� (22 Feb 2024 ~ Science) ‘Solving the puzzle of Long Covid’.

❦ Scientific Media Article ~ ‘Solving the puzzle of Long Covid’

By Al-Aly & Topol / Science ( 22 Feb 2024 ) [Abridged]

❦ ‘More than 4 years into the global COVID-19 pandemic, widespread infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has left millions of people around the world with Long Covid [ P ost- A cute S equelae of C OVID-19, or PASC ] , which describes the constellation of post-acute and long-term adverse health effects caused by the infection.

Evidence generated by the scientific community – with formidable contributions from patient-led research teams – has provided a thorough understanding of the epidemiology and clinical manifestations of Long Covid.

Understanding the biologic underpinnings of this disease is also improving, along with evidence that vaccination and antivirals can help prevent it.

Yet despite this progress, prevention efforts have stalled , there is uncertainty about governments ’ long-term commitment to address research needs in this area, and there has yet to be a treatment option validated with randomized controlled trials (RCTs).

‘Long Covid can manifest in people across the life span (from children to older adults ) and across race and ethnicity, sex, and baseline health status.

It is a complex non-monolithic , multi-systemic disease with sequelae across almost all organ systems .

The prototypical (classic) form of Long Covid (with brain fog [brain damage] , fatigue , dysautonomia , and post-exertional malaise ) is more common in younger adults and in females .

Other forms of Long Covid, including those with cardiovascular and metabolic sequelae , are manifest more often in older adults and those with comorbidities .’

In the post-acute phase of COVID-19, there was increased risk of an array of incident neurologic sequelae including:

✺ ischemic and hemorrhagic stroke;

✺ cognition and memory disorders;

✺ peripheral nervous system disorders;

✺ episodic disorders (for example, migraine and seizures);

✺ extrapyramidal and movement disorders;

✺ mental health disorders;

✺ musculoskeletal disorders;

✺ sensory disorders;

✺ Guillain–Barré syndrome;

✺ and encephalitis or encephalopathy.

‘ Regardless of age and across the age spectrum , people with COVID-19 had a higher risk of all the neurologic outcomes examined in this analysis.’

A common risk across all types of Long Covid is severity of acute infection ; the risk – on the relative scale – increases according to the severity of the acute infection .

‘However, despite the lower relative risk, more than 90% of [ Long Covid ] cases occur in people who had mild SARS-CoV-2 infection , owing to the much higher prevalence of mild cases.’

Because non-pharmaceutical interventions [ NPIs , such as respirator-wearing and air filtration ] to reduce the risk of SARS-CoV-2 transmission have largely been abandoned , vaccines are now the primary line of defense against both severe disease in the acute phase of the infection and Long Covid.

Studies have consistently shown that vaccines reduce the risk of Long Covid by 15% to 75% , with a mean of ~40% reduction in risk .

Yet vaccine policies in much of the world restrict boosters to older adults or those with risk factors for severe COVID-19, and with pandemic fatigue , the public’s appetite for boosters seems to be waning .

‘ Reinfection , which is now the dominant type of SARS-CoV-2 infection , is not inconsequential; it can trigger de novo Long Covid or exacerbate its severity .

Each reinfection contributes additional risk of Long Covid: cumulatively , two infections yield a higher risk of Long Covid than one infection , and three infections yield a higher risk than two infections .’

Despite this cumulative knowledge on mechanisms, epidemiology, and prevention, there are several major challenges.

Patients are often met with skepticism and dismissal of their symptoms as psychosomatic. The attribution of symptoms to psychological causes has no scientific support ; it perpetuates stigma and disenfranchises patients from accessing the care they need.

The lack of consensus on terms , definitions , and clinical trial end points for Long Covid is slowing progress and hampering industry engagement in clinical trials.

Evidence from multiple studies with 2 to 3 years of follow-up indicates prolonged risk for many sequelae and that spontaneous recovery or return to baseline status is uncommon .

Extended follow-up of the 1918 influenza pandemic , poliomyelitis outbreaks, and Epstein-Barr virus [ human herpesvirus 4, or HHV-4 ] infections has demonstrated that new , disabling sequelae of these infections can occur multiple decades later ; it is uncertain whether this will also occur with COVID-19.

‘Tied with the anti-science , anti-vaccine movement , a tide of Long Covid denialism is rising .’

This movement sows doubt about the scale and urgency of Long Covid, conflates Long Covid with vaccine-adverse events, and seeks to hamper progress on addressing the care needs of people suffering from this condition.

The pandemic has laid bare a blind spot in epidemiology and surveillance data systems for infectious diseases.

Nearly all surveillance data systems are built on the archaic , and now obsolete , notion that accounting for cases, hospitalization, and death in the acute phase is sufficient to capture the health burden of the infection.

This approach does not account for the burden of long-term health loss due to infectious illnesses, which obscures their true toll. Adding to this challenge are the absent , underdeveloped , or siloed healthcare data systems in much of the world.

Long Covid will have wide-reaching effects that are yet to be fully appreciated.

‘In addition to the prototypical form of Long Covid, SARS-CoV-2 infection increases the risk of a wide array of chronic diseases and will contribute to a rise in the burden of cardiovascular disease , diabetes , neurologic impairment , and autoimmune conditions .’

Long Covid affects the development and educational attainment of children and reduces labor participation and economic productivity in working-age adults .

Both the direct effect of increased risk of death in people with Long Covid, and the indirect effect on mortality through increased burden of chronic diseases caused by SARS-CoV-2 may contribute to further decline in life expectancy , potentially erasing decades of progress.

Finding treatments for Long Covid must be prioritized.

‘ Preventing infections and reinfections is the best way to prevent Long Covid and should remain the foundation of public health policy.’

A greater commitment to non-pharmaceutical interventions [ NPI s ] , which include masking [ N95/N99, or FFP2/FFP3/P3 respirators ] , especially in high-risk settings , and improved air quality through filtration and ventilation , are requisite .

Updating building codes to require mitigation against airborne pathogens and ensure safer indoor air should be treated with the same seriousness afforded to mitigation of risks from earthquakes and other natural hazards .

Reducing the risk of serious outcomes after COVID-19 and some prevention of Long Covid can be attained with vaccination of a wider spectrum of the population .

Development of more durable , variant-proof vaccines that are not vulnerable to evasion by the ever-mutating virus needs to be accelerated.

Nasally or orally administered vaccines that induce strong mucosal immunity to block infection and transmission should be pursued.

It is also necessary to broaden the pipeline of SARS-CoV-2 antivirals , especially because of rising resistance .’

❂

�� (22 Feb 2024 ~ Science) Solving the puzzle of Long Covid: Long Covid provides an opportunity to understand how acute infections cause chronic disease ➤

❂

✻ Medical notes:

The neurologic manifestations of Long Covid are hypothesized to be driven by neuro-inflammation with trafficking of immune cells (T cells and natural killer cells), cytokines and antibodies to the brain parenchyma resulting in activation of microglia and astrocytes, disturbances in synaptic signaling of upper-layer excitatory neurons, impaired neurogenesis and neuroblast formation, loss of oligodendrocytes and reduced myelinated axon density.

Other mechanisms may involve endothelial cell injury, complement activation and complement-mediated coagulopathy and microangiopathy leading to microbleeds or microclots.

Evidence from brain lysates of people with COVID-19 (compared with non-infected controls) demonstrates upregulation of transforming-growth-factor-beta signaling, hyperphosphorylation and post-translational modification of receptor and channel proteins typically linked to Alzheimer’s diseas e .

Legend: ‘Long Covid is a multi-systemic disease with sequelae that affect almost all organ systems.’

�� (22 Feb 2024 ~ Science) Solving the puzzle of Long Covid: Long Covid provides an opportunity to understand how acute infections cause chronic disease ➤

❦ Further Reading on Reinfections

�� (25 May 2022 ~ Nature Medicine) ‘Long COVID after breakthrough SARS-CoV-2 infection’. ➤

‘At 6 months after infection, beyond the first 30 days of illness, compared to contemporary controls, people with b reak t hrough SARS-CoV-2 i nfection (‘ BTI ’, or reinfection ) exhibited a higher risk of death and incident post-acute sequelae , including cardiovascular, coagulation and hematologic, gastrointestinal, kidney, mental health, metabolic, musculoskeletal and neurologic disorders.’

‘The development of new symptoms related to PCS [ Post-COVID-19 Syndrome / ‘Long Covid’ ] among participants initially recovered was associated with an intercurrent secondary SARS-CoV-2 infection [ reinfection ].’

More... PCS (PASC / ‘Long Covid’)

📖 Blood–brain barrier disruption and sustained systemic inflammation in individuals with long COVID-associated cognitive impairment

Thu, 22 Feb 2024 15:34:24 GMT

❦ “This study confirms everything that I have seen in the microscope over the last few years.

The authors of the study use a technique called dynamic contrast-enhanced magnetic resonance imaging ( DCE-MRI ), an imaging technique that can measure the density , integrity , and leakiness of tissue vasculature.

Comparing all individuals with previous COVID infection to unaffected controls revealed decreased general brain volume in patients with ‘brain fog’ – along with significantly reduced cerebral white matter volume in both hemispheres in the recovered and ‘brain fog’ cohorts .

Covid-19 induces brain-volume loss and leaky blood-brain barrier in some patients.

How can this be more clear?”

❂

�� (22 Feb 2024 ~ Nature: Neuroscience) Blood–brain barrier disruption and sustained systemic inflammation in individuals with long COVID-associated cognitive impairment ➤

‘ Our data suggest that sustained systemic inflammation and persistent localized blood-brain barrier (BBB) dysfunction is a key feature of long COVID-associated brain fog.

Patients with long COVID had elevated levels of IL-8, GFAP and TGFβ, with TGFβ specifically increased in the cohort with brain fog.

GFAP is a robust marker of cerebrovascular damage and is elevated after repetitive head trauma, reflecting BBB disruption, as seen in contact sport athletes and in individuals with self-reported neurological symptoms in long COVID.

Interestingly, TGFβ was strongly associated with BBB disruption and structural brain changes. ’

[Layperson overview] �� (February 2024 ~ Genetic Engineering and Biotechnology News) Leaky Blood Vessels in the Brain Linked to Brain Fog in Long COVID Patients ➤

[Related] �� (7 Feb 2022 ~ Nature: Cardiovascular Research) Blood–brain barrier link to human cognitive impairment and Alzheimer’s disease ➤

❂

✒ In History: Florence Nightingale’s ‘Notes on Nursing’ (1860)

Mon, 19 Feb 2024 23:52:12 GMT

‘The very first canon of nursing... the first essential to the patient... is this: to keep the air he breathes as pure as the external air, without chilling him .’

❂

Notes on Nursing (1860 edition)

By Florence Nightingale

First Published 1859. Revised edition reprinted in 1860 by Harrison of Pall Mall

Accessed 19 Feb 2024

❦ Chapter I – Ventilation and Warming

‘The very first canon of nursing, the first and the last thing upon which a nurse’s attention must be fixed, the first essential to the patient, without which all the rest you can do for him is as nothing, with which I had almost said you may leave all the rest alone, is this: TO KEEP THE AIR HE BREATHES AS PURE AS THE EXTERNAL AIR, WITHOUT CHILLING HIM.

Yet what is so little attended to?

Even where it is thought of at all, the most extraordinary misconceptions reign about it.

Even in admitting air into the patient’s room or ward, few people ever think where that air comes from.

It may come from a corridor into which other wards are ventilated, from a hall, always unaired, always full of the fumes of gas, dinner, of various kinds of mustiness; from an underground kitchen, sink, wash-house, water-closet, or even, as I myself have had sorrowful experience, from open sewers loaded with filth; and with this the patient’s room or ward is aired, as it is called – poisoned, it should rather be said.

Always air from the air without, and that, too, through those windows, through which the air comes freshest.

From a closed court, especially if the wind do not blow that way, air may come as stagnant as any from a hall or corridor.

I know an intelligent humane house surgeon who makes a practice of keeping the ward windows open.

The physicians and surgeons invariably close them while going their rounds; and the house surgeon, very properly, as invariably opens them whenever the doctors have turned their backs.

I have known a medical officer keep his ward windows hermetically closed, thus exposing the sick to all the dangers of an infected atmosphere, because he was afraid that, by admitting fresh air, the temperature of the ward would be too much lowered.

This is a destructive fallacy.

To attempt to keep a ward warm at the expense of making the sick repeatedly breathe their own hot, humid, putrescing atmosphere is a certain way to delay recovery or to destroy life.’

❂

‘I have known cases of hospital pyæmia quite as severe in handsome private houses as in any of the worst hospitals, and from the same cause, viz., foul air.

Yet nobody learnt the lesson.

Nobody learnt anything at all from it.’

❂

✪ C-19: On schools

‘Of all places, public or private schools, where a number of children or young persons sleep in the same dormitory * , require this test of freshness to be constantly applied.’

* [ C-19 Note: You might substitute ‘sleep’ and ‘dormitory’ with ‘study’ and ‘classroom’ in this section.]

‘If it be hazardous for two children to sleep together in an unventilated bedroom, it is more than doubly so to have four, and much more than trebly so to have six under the same circumstances.

People rarely remember this; yet, if parents were as solicitous about the air of school bedrooms as they are about the food the children are to eat, and the kind of education they are to receive, at school, depend upon it due attention would be bestowed on this vitally important matter, and they would cease to have their children sent home either ill, or because scarlet fever or some other “current contagion” had broken out in the school.

There are schools where attention is paid to these things, and where “children’s epidemics” are unknown.’

❂

✪ C-19: Offices, shops, factories, and other workplaces

‘How much sickness, death, and misery are produced by the present state of many factories, warehouses, workshops, and workrooms!’

‘How much sickness, death, and misery are produced by the present state of many factories, warehouses, workshops, and workrooms!

The places where poor dressmakers, tailors, letter-press printers, and other similar trades have to work for their living, are generally in a worse sanitary condition than any other portion of our worst towns.

Many of these places of work were never constructed for such an object. They are badly adapted garrets, sitting-rooms, or bedrooms, generally of an inferior class of house.

No attention is paid to cubic space or ventilation.

The poor workers are crowded on the floor to a greater extent than occurs with any other kind of over-crowding.

The constant breathing of foul air, saturated with moisture, and the action of such air upon the skin renders the inmates peculiarly susceptible of the impression of cold, which is an index indeed of the danger of pulmonary disease to which they are exposed.

The result is, that they make bad worse, by over-heating the air and closing up every cranny through which ventilation could be obtained.

In such places, and under such circumstances of constrained posture, want of exercise, hurried and insufficient meals, long exhausting labour and foul air – is it wonderful that a great majority of them die early of chest disease, generally of consumption?

Intemperance is a common evil of these workshops.

The men can only complete their work under the influence of stimulants, which help to undermine their health and destroy their morals, while hurrying them to premature graves.

Employers rarely consider these things.

Healthy workrooms are no part of the bond into which they enter with their work-people. They pay their money, which they reckon their part of the bargain.

And for this wage the workman or workwoman has to give work, health, and life.

Do men and women who employ fashionable tailors and milliners ever think of these things?

And yet the master is no gainer.

His goods are spoiled by foul air and gas fumes, his own health and that of his family suffers, and his work is not so well done as it would be, were his people in health.

And the time will come when it will be found cheaper to supply shops, warehouses, and work-rooms with pure air than with foul air.’

‘And the time will come when it will be found cheaper to supply shops, warehouses, and work-rooms with pure air than with foul air.’

❂

✪ C-19: On ‘air-tests’, and measuring CO₂ as a proxy for estimating prevalence of airborne disease indoors

‘Dr. Angus Smith’s air-test, if it could be made of simple application, would be invaluable to use in every sleeping and sick room.

Just as without the use of a thermometer no nurse should ever put a patient into a bath, so, if this air-test were made in some equally simple form, should no nurse, or mother, or superintendent, be without it in any ward, nursery, or sleeping-room.

But to be used, the air-test must be made as simple a little instrument as the thermometer, and both should be self-registering.

‘...the air-test must be made as simple a little instrument as the thermometer, and both should be self-registering.’

The senses of nurses and mothers become so dulled to foul air that they are perfectly unconscious of what an atmosphere they have let their children, patients, or charges sleep in.

But if the tell-tale air-test were to exhibit in the morning, both to nurses and patient and to the superior officer going round, what the atmosphere has been during the night, I question if any greater security could be afforded against a recurrence of the misdemeanour.’

❂

✪ C-19: ... And back to the school-room, testing its air, and combatting airborne pathogens

‘And, oh! the crowded national school! where so many children’s epidemics have their origin; and the crowded, unventilated work-room, which sends so many consumptive men and women to the grave; what a tale its air-test would tell!

We should have parents saying, and saying rightly, “I will not send my child to that school. I will not trust my son or my daughter in that tailor’s or milliner’s workshop, the air-test stands at ‘Horrid.’”

‘We should have parents saying, and saying rightly, “I will not send my child to that school... the air-test stands at Horrid .”’

And the dormitories of our great boarding schools!

Scarlet fever would be no more ascribed to contagion but to its right cause, the air-test standing at “Foul.”

We should hear no longer of “mysterious dispensations,” nor of “plague and pestilence” being “in God’s hands,” when, so far as we know, He has put them into our own.

The little air-test would both betray the cause of these “mysterious pestilences,” and call upon us to remedy it.’

❂

❦ Chapter II – Health of Houses

‘There are five essential points in securing the health of houses:–

Pure air.

Pure water.

Efficient drainage.

Cleanliness.

Light.

Without these, no house can be healthy. And it will be unhealthy just in proportion as they are deficient.

To have pure air, your house must be so constructed as that the outer atmosphere shall find its way with ease to every corner of it.

‘To have pure air, your house must be so constructed as that the outer atmosphere shall find its way with ease to every corner of it.’

House architects hardly ever consider this.

The object in building a house is to obtain the largest interest for the money, not to save doctor’s bills to the tenants.

But, if tenants should ever become so wise as to refuse to occupy unhealthily constructed houses, and if Insurance Companies should ever come to understand their interest so thoroughly as to pay a Sanitary Surveyor to look after the houses where their clients live, speculative architects would speedily be brought to their senses.

As it is, they build what pays best. And there are always people foolish enough to take the houses they build.

And if in the course of time the families die off, as is so often the case, nobody ever thinks of blaming any but Providence for the result.

Ill-informed medical men aid in sustaining the delusion, by laying the blame on “current contagions”.

Badly constructed houses do for the healthy what badly constructed hospitals do for the sick.’

‘Badly constructed houses do for the healthy what badly constructed hospitals do for the sick.’

❂

❦ Conclusion

‘The whole of the preceding remarks apply even more to children and to puerperal women than to patients in general.

They also apply to the nursing of surgical, quite as much as to that of medical cases. Indeed, if it be possible, cases of external injury require such care even more than sick.

In surgical wards, one duty of every nurse certainly is prevention.

Fever, or hospital gangrene, or pyæmia, or purulent discharge of some kind may else supervene.

If she allows her ward to become filled with the peculiar close fœtid smell, so apt to be produced among surgical cases, especially where there is great suppuration and discharge, she may see a vigorous patient in the prime of life gradually sink and die where, according to all human probability, he ought to have recovered.

The surgical nurse must be ever on the watch, ever on her guard, against want of cleanliness, foul air, want of light, and of warmth.’

‘In surgical wards, one duty of every nurse certainly is prevention.’

❂

�� (Accessed 19 Feb 2024 ~ Original text copied from FiftyWordsForSnow.com) Notes on Nursing (1860) ➤

�� (Accessed 19 Feb 2024 ~ Original scanned pages from Google Books) Notes on Nursing (1860) ➤

❂

Notes on the 1859 versus the 1860 editions of ‘Notes on Nursing ’ by Florence Nightingale (Accessed 19 Feb 2024 ~ Cambridge University Press) ➤

Nightingale wrote ‘Notes on Nursing’ – first published in 1859, but reprinted in its revised and enlarged 1860 edition – in order to share her knowledge with women who were nursing their families at home.

❦ Carbon dioxide (CO₂) monitor with app

‘... the air-test must be made as simple a little instrument as the thermometer, and both should be self-registering...’

The industry-standard CO₂ monitor with app: the Aranet4 Home. Review by HouseFresh.com ➤ .

Aranet4 Home at Amazon.co.uk.

Custom decal by Amanda Hu .

❦ Assessing air quality in a classroom by measuring CO₂ as a proxy for airborne disease

‘We should have parents saying, and saying rightly, “I will not send my child to that school... the air-test stands at Horrid...”’

❦ Environment Code (2022): Air Renewal in French Schools

❦ ‘Environment Code (2022): Air Renewal in French Schools’.

⚒ Resource: LitCovid ~ SARS-CoV-2 / COVID-19 Literature Hub

Sun, 18 Feb 2024 15:19:52 GMT

❦ LitCovid is the most comprehensive online resource on SARS-CoV-2 / COVID-19, providing access to 417,800+ relevant articles on PubMed.

The library of scientific articles is updated daily, and categorised by different research topics (e.g. transmission), as well as geographic locations.

➲ Date accessed: 18 Feb 2024 .

❂

❦ Useful Categories

✪ Transmission ➤

Characteristics and modes of SARS-CoV-2 transmission.

✪ Prevention ➤

Prevention, control, response and management strategies.

✪ Long Covid ➤

Post-COVID-19 Conditions/Complications (PCC) / Post-Acute Sequelae of COVID-19 (PASC).

✪ Case Reports ➤

Descriptions of specific patient cases.

✪ Treatments ➤

Treatment strategies, therapeutic procedures, and vaccine development.

✪ Forecasting ➤

Modelling, and estimating the trend of SARS-CoV-2 spread.

❂

➲ LitCovid Online Library ➤

A Top Ten COVID-19 Mitigation Wishlist ~ or How to Turn a Country Around

Sat, 17 Feb 2024 15:43:42 GMT

❦ Mitigation = ‘Lessening the force or intensity of something unpleasant; the act of making a condition or consequence less severe.’

1. Clean indoor air .

The priority should be air filters in schools and hospitals .
New ventilation and air filtration standards for all public spaces .
Grants made available to businesses to upgrade ventilation and air filtration .

2. FFP2/3 [N95/N99] respirators (masks) in all healthcare settings .

3. Free Covid vaccines available to everyone.

4. Wider access to Covid anti-viral treatments .

5. Free LFT/PCR testing .

6. Improved Covid surveillance , including wastewater monitoring and Long Covid prevalence .

7. Paid sick-leave , so that people don’t go to work when ill.

8. Respirators (masks) on public transport , including flights .

9. Better support and treatments for Long Covid patients .

... and last, but by no means least:

10. A public education campaign on the long-term risks of Covid – and why people should do more to protect themselves.

❦ Addendum :

Allocate adequate research funding for a sterilising vaccine as well as treatments/cure for Long Covid .

❂

📖 Long-term risks of respiratory diseases in patients infected with SARS-CoV-2: a longitudinal, population-based cohort study

Sat, 17 Feb 2024 13:54:10 GMT

❦ ‘The occurrences of respiratory disorders among patients who survived for 30 days after the COVID-19 diagnosis continued to rise consistently, including asthma , bronchiectasis , COPD , ILD , PVD * , and lung cancer .

* COPD = Chronic obstructive pulmonary disease .

ILD = Interstitial lung disease .

PVD = Peripheral vascular disease .

With the severity of the acute phase of COVID-19, the risk of all respiratory diseases increases progressively.

Besides, during the 24-months follow-up, we observed an increasing trend in the risks of asthma and bronchiectasis over time, which indicates that long-term monitoring and meticulous follow-up of these patients is essential.

These findings contribute to a more complete understanding of the impact of COVID-19 on the respiratory system and highlight the importance of prevention and early intervention of these respiratory sequelae of COVID-19.

In this study, several key findings have been further identified.

Firstly, our research demonstrates a significant association between COVID-19 and an increased long-term risk of developing various respiratory diseases.

Secondly, we found that the risk of respiratory disease increases with severity in patients with COVID-19, indicating that it is necessary to pay attention to respiratory COVID-19 sequelae in patients, especially those hospitalized during the acute stage of infection.

This is consistent with the findings of Lam et al., who found that the risk of some respiratory diseases (including chronic pulmonary disease, acute respiratory distress syndrome and ILD) increased with the severity of COVID-19.

Notably, however, our study found that asthma and COPD remained evident even in the non-hospitalized population.

This emphasizes that even in cases of mild COVID-19, the healthcare system should remain vigilant.

Thirdly, we investigated differences in risk across time periods, as well as the long-term effects of COVID-19 on respiratory disease.

During the 2-years follow-up period, the risks of COPD, ILD, PVD and lung cancer decreased, while risks of asthma and bronchiectasis increased.

Fourthly, our study showed a significant increase of the long-term risk of developing asthma, COPD, ILD, and lung cancer diseases among individuals who suffered SARS-CoV-2 reinfection.

This finding emphasizes the importance of preventing reinfection of COVID-19 in order to protect public health and reduce the potential burden of SARS-CoV-2 reinfection.

Interestingly, vaccination appears to have a potentially worsening effect on asthma morbidity compared with other outcomes.

This observation aligns with some previous studies that have suggested a possible induction of asthma onset or exacerbation by COVID-19 vaccination.

It suggests that more care may be necessary for patients with asthma on taking the COVID vaccines.

The underlying mechanisms associated with COVID and respiratory outcomes are not fully understood, but several hypotheses have been proposed.

First, SARS-CoV-2 can persist in tissues (including the respiratory tract), as well as the circulating system for an extended period of time after the initial infection.

This prolonged presence of the virus could directly contribute to long-term damage of the respiratory tissues, consequently leading to the development of various respiratory diseases.

Second, it has been observed that SARS-CoV-2 infection can lead to prolonged immunological dysfunctions, including highly activated innate immune cells, a deficiency in naive T and B cells, and increased expression of interferons and other pro-inflammatory cytokines.

These immune system abnormalities are closely associated with common chronic respiratory diseases – asthma, bronchiectasis, COPD, as well as the development of lung cancer.

Next, SARS-CoV-2 itself has been shown to drive cross-reactive antibody responses, and a range of autoantibodies were found in patients with COVID-19.

In conclusion, our research adds to the existing knowledge regarding the effects of COVID-19 on the respiratory system.

Specifically, it shows that the risk of respiratory illness increases with the severity of infection and reinfection.

Our findings emphasize the importance of providing extended care and attention to patients previously infected with SARS-CoV-2.’

❂

�� (17 Feb 2024 ~ The Lancet: eClinical Medicine) Long-term risks of respiratory diseases in patients infected with SARS-CoV-2: a longitudinal, population-based cohort study ➤

On the perfect medical crime

Fri, 09 Feb 2024 18:10:42 GMT

❦ “Chronic disease is like the perfect medical crime.

The cause is usually long gone by the time the disease manifests, and nobody links the two until it’s much too late for most.”

❂

On unseen costs, refrigerator trucks, and the train coming down the tunnel

Sat, 27 Jan 2024 20:05:38 GMT

❦ “It’s really not in the interest of the virus to kill us quickly.

That’s why it has mutated to immune escape. That way it enters silently, and then eats you slowly whilst you’re still a spreading vector.

Refrigerator trucks are long gone. That’s all the political class wanted.

The unseen costs of CVD [cardiovascular disease] , DM [diabetes mellitus] , and both dementia and Parkinson’s Disease are the train coming down the tunnel.

The economists are catching up. The actuaries are already there.

Politicians and most people? Not yet...”

❂

On shock treatment

Mon, 22 Jan 2024 14:48:01 GMT

❦ “I was in hospital for tests this morning. A nurse asked me:

— “How come so many people are wearing masks? Is there something I don’t know?”

I almost lost the power of speech.”

✾

⚒ Resource: Genomic Mapping of SARS-CoV-2 / COVID-19 Variants

Sun, 21 Jan 2024 16:02:59 GMT

❦ Genomic epidemiology of SARS-CoV-2 with subsampling focused globally since pandemic start.

‘A quantum leap of SARS-CoV-2 evolution was observed on two occasions .

The first occurred at the end of 2021 , when the highly mutated Omicron variant ( B.1.1.529 ) became dominant, showing unprecedented antibody evasion .

The second major evolutionary shift was observed in July 2023 , when the subvariant BA.2.86 – a highly mutated descendant of the BA.2 variant – emerged and dominated globally in 2024 .’

❦ By Tree (Unrooted) .

➲ Accessed: 21 January 2024 .

❦ By Tree (Unrooted) .

➲ Accessed: 29 October 2024 .

➲ See current: By Tree (Unrooted) ➤

‘ Before Omicron , natural infection provided strong and durable protection against reinfection , with minimal waning over time.

However, during the Omicron era, protection was robust only for those recently infected , declining rapidly over time and diminishing within a year .’

❦ By Date .

➲ Accessed: 7 September 2025 .

➲ See current: By Date ➤

‘ Vaccine effectiveness against SARS-CoV-2 [ COVID-19 ] infection declines markedly with time and Omicron variants .’

❦ By Mutation .

➲ Accessed: 21 January 2024 .

❦ By Mutation .

➲ Accessed: 15 March 2025 .

➲ See current: By Mutation ➤

‘The average interval for SARS-CoV-2 [ COVID-19 ] reinfection was 149.91 days .

❦ By Tree (Radial) .

➲ Accessed: 21 January 2024 .

❦ By Tree (Radial) .

➲ Accessed: 29 October 2024 .

❦ By Tree (Radial) .

➲ Accessed: 29 September 2025 .

➲ See current: By Tree (Radial) ➤

Data

➲ Built with nextstrain/ncov . Maintained by the Nextstrain team . Enabled by data from GISAID .

“ If you are letting yourself get infected and taking no precautions against passing it on, you are not a passive bystander for your next infection.

You’ve participated in creating it. ”

Dr. Noor Bari, Emergency Medicine (2024) ➲

More... On Variants

More... On Transmission

On nosocomial (hospital-acquired or healthcare-associated) infection (HAI)

Sat, 20 Jan 2024 15:22:34 GMT

❦ “Every single case in which a person with COVID-19 infects another person in a healthcare setting – patient, relative, or hospital staff member – is a significant failure of hospital procedures.

Every single instance .”

✾

⚒ Resource: SARS-CoV-2 / COVID-19 Genomic Sequence Variant Visualiser

Fri, 19 Jan 2024 20:03:37 GMT

❦ Mike Honey’s Variant Visualiser (COVID-19 Genomic Sequence Analysis).

The region of ‘Oceania/Australia’ is set by default, as the visualiser was created by Mike Honey , a Data Visualisation and Data Integration specialist in Melbourne, Australia.

➲ Choose your country by clicking on the ‘ Continent, Country, Location ’ dropdown menu in the top-right-hand corner .

The variant visualiser is free to use, and is automatically updated every time you open the link.

❂

❦ Screenshot of the Variant Visualiser showing SARS-CoV-2 sub-/variants active in the United Kingdom from 1 Nov 2023 – 9 Jan 2024 .

➲ Data accessed: 19 Jan 2024 .

❦ Screenshot of the Variant Visualiser showing SARS-CoV-2 sub-/variants active in the United Kingdom from 1 Jul 2023 – 13 Sep 2023 .

➲ Data accessed: 13 Sep 2023 .

More... ⚒ Resources

📖 Microstructural brain abnormalities, fatigue, and cognitive dysfunction after mild COVID-19

Fri, 19 Jan 2024 15:30:27 GMT

❦ ‘Although some studies have shown neuroimaging and neuropsychological alterations in post-COVID-19 patients, fewer combined neuroimaging and neuropsychology evaluations of individuals who presented a mild acute infection.

Here we investigated cognitive dysfunction and brain changes in a group of mildly infected individuals.

We conducted a cross-sectional study of 97 consecutive subjects ( median age of 41 years ) without current or history of psychiatric symptoms (including anxiety and depression) after a mild infection , with a median of 79 days (and mean of 97 days ) after diagnosis of COVID-19.

We performed semi-structured interviews, neurological examinations, 3T-MRI scans, and neuropsychological assessments.

The patients reported memory loss ( 36% ), fatigue ( 31% ) and headache ( 29% ).

The quantitative analyses confirmed symptoms of fatigue ( 83% of participants), excessive somnolence ( 35% ), impaired phonemic verbal fluency ( 21% ), impaired verbal categorical fluency ( 13% ) and impaired logical memory immediate recall ( 16% ).

Our group… presented higher rates of impairments in processing speed ( 11.7% in FDT- Reading and 10% in FDT- Counting ).

The white matter (WM) analyses with DTI * revealed higher axial diffusivity values in post-infected patients compared to controls.

* Diffusion tensor imaging tractography , or DTI tractography, is an MRI (magnetic resonance imaging) technique most commonly used to provide imaging of the brain.

Our results suggest persistent cognitive impairment and subtle white matter abnormalities in individuals mildly infected , without anxiety or depression symptoms.

One intriguing fact is that we observed a high proportion of low average performance in our sample of patients (which has a high average level of education ), including immediate and late verbal episodic memory, phonological and semantic verbal fluency, immediate visuospatial episodic memory, processing speed, and inhibitory control .

Although most subjects did not present significant impaired scores compared with the normative data, we speculate that the low average performance affecting different domains may result in a negative impact in everyday life , especially in individuals with high levels of education and cognitive demands .’

❂

❦ Note how these findings might negatively affect daily activities that demand sustained cognitive attention and fast reaction times – such as driving a car or motorbike, or piloting a plane. Consider air-traffic control.

Consider the impact on healthcare workers whose occupations combine long periods of intense concentration with a need for critical precision.

❂

�� (19 Jan 2024 ~ Nature: Scientific Reports) Microstructural brain abnormalities, fatigue, and cognitive dysfunction after mild COVID-19 ➤

On bone health, bone loss, and vertebral fractures ~ 📖 SARS-CoV-2 and its Multifaceted Impact on Bone Health: Mechanisms and Clinical Evidence

Thu, 18 Jan 2024 20:37:51 GMT

‘ Clinical evidence suggests that SARS-CoV-2 may lead to hypocalcemia, altered bone turnover markers, and a high prevalence of vertebral fractures. ’

�� (18 Jan 2024 ~ Current Osteoporosis Reports) ‘ SARS-CoV-2 and its Multifaceted Impact on Bone Health: Mechanisms and Clinical Evidence ’.

❦ Study ~ ‘SARS-CoV-2 and its Multifaceted Impact on Bone Health: Mechanisms and Clinical Evidence’

By Harris et al / Current Osteoporosis Reports ( 18 Jan 2024 )

❦ ‘As part of the post-acute sequelae of SARS-CoV-2 infection, bone health changes are affected by COVID-19 both directly and indirectly, with multiple potential mechanisms and risk factors involved.

In vitro and pre-clinical studies suggest that SARS-CoV-2 may directly infect bone marrow cells, leading to alterations in bone structure and osteoclast numbers.

The virus can also trigger a robust inflammatory response, often referred to as a ‘cytokine storm’, which can stimulate osteoclast activity and contribute to bone loss.

‘ Clinical evidence suggests that SARS-CoV-2 may lead to hypocalcemia, altered bone turnover markers, and a high prevalence of vertebral fractures. ’

Furthermore, disease severity has been correlated with a decrease in bone mineral density.

Indirect effects of SARS-CoV-2 on bone health, mediated through muscle weakness, mechanical unloading, nutritional deficiencies, and corticosteroid use, also contribute to the long-term consequences.

The interplay of concurrent conditions such as diabetes, obesity, and kidney dysfunction with SARS-CoV-2 infection further complicates the disease’s impact on bone health.’

❂

�� (18 Jan 2024 ~ Current Osteoporosis Reports) ‘S ARS-CoV-2 and its Multifaceted Impact on Bone Health: Mechanisms and Clinical Evidence ’.

Figure 1: ‘Overview of mechanisms through which SARS-CoV-2 can cause bone loss.’ ➤

�� (18 Jan 2024 ~ Current Osteoporosis Reports) SARS-CoV-2 and its Multifaceted Impact on Bone Health: Mechanisms and Clinical Evidence ➤

❂

More... Musculoskeletal: Bones & Muscles

More... PASC (‘Long Covid’)

On individual risk assessment vs. public health bodies, and the WHO

Thu, 18 Jan 2024 16:12:57 GMT

❦ “We cannot individually assess the risk of infection from poor indoor air quality (IAQ).

Just as we cannot individually assess food safety in restaurants, or fire safety in cinemas, or aviation safety on flights.

These are in the control of others, and are regulated for our health and safety.”

From WHO (Europe):

❦ ‘No-one knows your risk like you yourself do.

What we need to do now is apply that knowledge when and where it matters.

This means assessing our own level of risk and our risk to others at every step of our days.

And then apply the protective measures that matter most to reduce the chances of catching or spreading respiratory infections.

Measures range from staying at home if sick, hand and cough hygiene, and adequate indoor ventilation; to mask-wearing in certain settings – such as hospitals or crowded places.

In this context, we all need to use our own judgement when taking steps to protect ourselves, and others around us, based on an individual assessment of risk.’

✾

“Coughing into one’s sleeve while in shared air is like peeing into one’s swimsuit while in shared water.”

“There is no such thing as ‘personal risk assessment’ for the vast majority of people.

A tiny number of dominant personalities in your life (and it could be you) have decided what to do, and the rest will follow...”

Dr. Noor Bari, Emergency Medicine (2023) ➲

Studies, articles & comment on... Airborne SARS-CoV-2 transmission

📖 Immune damage in Long Covid

Thu, 18 Jan 2024 13:07:44 GMT

❦ ‘Acute infections with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) cause a respiratory illness that can be associated with systemic immune cell activation and inflammation , widespread multi-organ dysfunction , and thrombosis .

Not everyone fully recovers from COVID-19, leading to Long Covid, the treatment of which is a major unmet clinical need.

Long Covid can affect people of all ages , follows severe as well as mild disease , and involves multiple organs .

Patients with Long Covid display signs of immune dysfunction and exhaustion , persistent immune cell activation , and autoimmune antibody production , which are also pathological features of acute COVID-19.

The complement system is crucial for innate immune defense by effecting lytic destruction of invading micro-organisms, but when uncontrolled, it causes cell and vascular damage .

The complement cascade is activated by antigen–antibody complexes in the classical pathways or in the lectin pathway by multimeric proteins (lectins) that recognize specific carbohydrate structures, which are also found on the SARS-CoV-2 spike protein that facilitates host cell entry.

Both pathways may contribute to the pronounced complement activation in acute COVID-19.

Long Covid symptoms include a postexertional exhaustion reminiscent of other post-viral illnesses , such as myalgic encephalomyelitis ( ME ) – chronic fatigue syndrome ( MECFS ) with suspected latent viral reactivation .

Antibody titer changes in Long Covid patients indicate an association of fatigue with reactivation of latent Epstein-Barr virus ( EBV ) infections , and Cervia-Hasler et al found that the severity of Long Covid symptoms is associated with cytomegalovirus ( CMV ) reactivation .

A better understanding of the connections between viral reactivation, persistent interferon signaling, and autoimmune pathologies promises to yield new insights into the thromboinflammation associated with Long Covid.

Although therapeutic interventions with coagulation and complement inhibitors in acute COVID-19 produced mixed results, the pathological features specific for Long Covid suggest potential interventions for clinical testing.

Microclots are also observed in ME-CFS patients , indicating crucial interactions between complement, vWF, and coagulation-mediated fibrin formation in post-viral syndromes.

A better definition of these interactions in preclinical and clinical settings will be crucial for the translation of new therapeutic concepts in chronic thromboinflammatory diseases .’

❂

�� (18 Jan 2024 ~ Science) Immune damage in Long Covid ➤

Complement-coagulation cross-talk at the endothelial interface.

During acute COVID-19, the complement and coagulation systems can become activated, and remain locally activated in various tissues in Long Covid patients.

Endothelial cell damage by membrane insertion of the complement C5b-C7 complex results in vWF and TSP1 release.

This is highly prothrombotic because the resulting vWF multimers recruit platelets and promote thrombin generation, and TSP1 promotes monocyte interactions with platelets.

Additionally, reduced ADAMTS13 in Long Covid patients promotes the accumulation of ultralarge vWF multimers, which induces C3b binding and stimulates the alternative pathway of complement activation.

Together, these feedback loops can maintain local complement activation and inflammation, as well as generating microclots that could underlie some of the features of Long Covid .

�� (18 Jan 2024 ~ Science) Immune damage in Long Covid ➤

📖 Beyond breathing: How COVID-19 affects your heart, brain and other organs

Tue, 16 Jan 2024 07:29:30 GMT

“I would argue that COVID-19 is not a disease of the lungs at all.

It seems most likely that it is what we call a vascular and neurologic infection, affecting both nerve endings and our cardiovascular system.”

�� (16 Jan 2024 ~ American Heart Association) ‘Beyond breathing: How COVID-19 affects your heart, brain and other organs’.

❦ Scientific Media Article ~ ‘Beyond breathing: How COVID-19 affects your heart, brain and other organs’

By Michael Merschel / American Heart Association ( 16 Jan 2024 )

❦ ‘The (2023-2024) New Year started with an increase in COVID-19 hospitalizations in the U.S., prompting Hernandez and other experts to advise caution , especially for those at high risk .

While the short-term effects of COVID-19 can be flu-like , even mild cases can lead to long COVID [ Post-Acute Sequelae of COVID-19, or PASC ] .

Because COVID-19 typically affects breathing and can lead to problems such as pneumonia, many people may think it’s primarily a lung disease.

It’s not that simple, said Dr. Nisha Viswanathan, director of the long COVID program at the David Geffen School of Medicine at the University of California, Los Angeles.

“I would argue that COVID-19 is not a disease of the lungs at all,” she said.

“It seems most likely that it is what we call a vascular and neurologic infection , affecting both nerve endings and our cardiovascular system .”

It’s no surprise that experts say SARS-CoV-2 – the name of the virus that causes COVID-19 – is complex, with many of its pathways just beginning to be understood. But some things are becoming clear.

One of the best reviews of long COVID symptoms appeared last January [ 2023 ] in Nature Reviews Microbiology. It detailed the disease’s effects throughout the body , including the pancreas , blood vessels and reproductive system .

“ SARS-CoV-2 is excellent at triggering your immune system to go from zero to 100 ,” said Dr. Lindsay McAlpine, a neurologist who is director of the Yale NeuroCovid Clinic.

That revving of the immune response leads to both a “ wide swath of inflammation ” and excessive blood clotting .

“Perhaps the viral replication is going on in the lungs and nasopharynx [ the area at the top of the throat that connects the nose to the respiratory system ] . But the inflammation that the virus triggers is systemic .”

❦ The brain & nervous system

“The virus and the immune response can have several different effects on the brain ,” said McAlpine, lead author of a 2021 study looking at ischemic strokes in people with COVID-19 .

The exact causes of brain-related issues are not clear, but she said it does not appear that the virus is directly attacking brain tissue.

‘Rather, it seems that the ramped-up immune response leads to clots that could cause brain problems .’

“In addition to the cognitive impairment , we see worsening or new-onset migraines ,” she said. “We see new neuropathy in the legs and the arms – numbness , tingling , difficulty walking because of the neuropathy.”

COVID-19 might also be unmasking other neurodegenerative conditions, such as Parkinson’s disease , she said. McAlpine has diagnosed new cases of Alzheimer’s disease in people who, before COVID-19, were functioning fine, then developed symptoms.

❦ The heart & blood vessels

The risk of dangerous clotting – including deep vein thrombosis ( clots in large veins ) and pulmonary embolisms ( clots in the lungs ) – is small but stays elevated for up to a year after the infection .

Many factors might be playing into COVID-related heart problems , including microclots – tiny blood clots – or an autoimmune response targeting heart muscle cells.

A recent study in Nature Cardiovascular Research shows the virus may infect coronary arteries , causing plaque build-up to become inflamed and break off, which can lead to a heart attack .

❦ The Gastrointestinal system

“Interestingly, the GI system’s mechanism may be a little different than what impacts the heart,” Viswanathan said. One theory suggests that the virus finds a [ ‘safe’ ] hiding place while the rest of the body fights it off.

“And we have found now in multiple studies that COVID can remain in our GI tract for weeks and months after it has resolved in the rest of the body.”

The exact place where the virus might hide is up for debate. But gastrointestinal symptoms are clear: “People can have nausea , vomiting , diarrhea .”

A large study of veterans published last year [ 7 Mar 2023 ] in Nature Communications found people with COVID-19 had a higher risk of gastroesophageal reflux disease , irritable bowel syndrome and other gastrointestinal problems more than 30 days after infection compared to people without COVID-19.

The risk was elevated even among people who had mild cases of the disease.

❦ The Kidneys

Kidney problems were common in a 2023 study published in The Lancet Respiratory Medicine that looked at organ damage after COVID-19 infection.

❦ What to do?

The first step is to be cautious if COVID-19 is surging in your area. Consider wearing a mask in crowded public places.

[If you don’t want repeat reinfections , and their cumulatively higher risk of life-altering or fatal consequences , wear a well-fitting ( N95/N99 or FFP2/FFP3 ) respirator in all public spaces , particularly in the highest-risk settings of healthcare , education and transport .]

“A lot of people have COVID now, and it may take a while for them to test positive.

The second thing is get vaccinated.”

The [ USA’s ] Centers for Disease Control and Prevention recommends everyone ages 5 and older get the updated COVID-19 vaccine to avoid getting seriously ill from the virus. *

* [ Pre-2025 Trump election in the USA. Pre-2024 Summer / Autumn / Winter cancellation of SARS-CoV-2 vaccines for those aged 50-plus in the UK .]

“The third thing is controlling your cardiovascular risk factors,” she said. That means getting high blood pressure, diabetes or other chronic medical conditions under control.

McAlpine added that if you have COVID-19 symptoms , stay away from other people to avoid putting them at risk .

“And if you could avoid an illness like COVID or the flu – why wouldn’t you?”’

❂

�� (16 Jan 2024 ~ American Heart Association) Beyond breathing: How COVID-19 affects your heart, brain and other organs ➤

‘Beyond breathing: How COVID-19 affects your heart, brain and other organs.’

❦ Further reading on the heart

(25 Feb 2025 ~ C19.Life) ‘ The beating heart... 70 studies and articles on SARS-CoV-2 and the cardiovascular system (2020–2024) ➲ ’.

❂

‘ Results from this study indicated a statistically significant increased risk for a range of cardiovascular conditions as well as mortality.

While these risks were heightened for individuals who experienced a more severe acute episode of COVID-19 (ie. requiring hospitalization), it is essential to note that most individuals ( 72.5% ) in the cohort did not experience hospitalization during the acute phase.

Many of these conditions will have lasting effects on quality of life. ’ ➤

❂

More... Cardiovascular system

On cardiac bedside chats, clean air, SARS-CoV-2 transmission, and breaches of UK legislation in the workplace

Tue, 09 Jan 2024 16:43:09 GMT

❦ “I met a nice lady – a ward patient – yesterday who, seeing my [ FFP3 ] respirator [ high-filtration ‘mask’ ] , promptly put on her surgical mask.

So instead of diving straight in to asking what was most concerning her and how I could help, I opened up a bit about infection control in hospitals.

I explained how, because of a lack of respirators, March 2020 saw NHS leaders downgrade PPE for all non-ICU staff.

❂ PPE : Personal Protective Equipment.

I then reminded her of the amazing DHSC 2020 and 2021 campaigns on airborne transmission of SARS2 (the green-and-black smoke ones) – and I had to point out that every IPC Lead Nurse had since had to switch off their brain and forget what they knew – and while at work, to only protect ICU staff.

❂ DHSC : Department of Health and Social Care (UK).

❂ IPC : Infection Prevention and Control.

I explained that the individuals responsible for the original IPC downgrade were now authors of the national manual on IPC (NIPCM), which sets the standard for infection control in hospitals, and this manual states that airborne transmission is ‘not a thing’ for SARS2 (AGP only).

❂ NIPCM : The UK’s National Infection Prevention and Control Manual.

❂ AGP : Aerosol-Generating Procedure, ie. intubation.

So hospitals are destined to be unsafe spaces thanks to the NIPCM, and the surgical mask that she was wearing was OK (ish) to help protect me – but did very little to reduce her risk of SARS2 inhalation.

However, she was in a single room (an extra, and not meant as a ward-bed space – but you know, >100% occupancy forever means that you need to use your imagination) – and she already had the window open.

She was appalled at what healthcare workers were being put through.

She was appalled at the on-going lies.

She was appalled at the possible level of harm to patients and staff from such lies.

She then went on to tell me how a weekend visitor of hers had just tested positive for Covid.

She was worried that they had hugged and chatted, and that she might have got infected.

She’s a switched on lady, too. Lives with a medic who has the windows open all the time (“It’s freezing at home”).

So I explained about the CleanAirStars.com site.

About HEPA filtration being a low energy and low-cost way to remove all airborne pathogens , and to make home a safer place for...

• Covid
• Flu
• RSV
• Norovirus
• Fungi, etc. etc.

The list goes on and on.

— “Wow, that’s like magic!”

We had a very nice chat. And then we talked about her heart.

I just wish I could have this same conversation with each and every NHS CEO and IPC Lead Nurse.

I’d ask some questions.

I’d want to know why they aren’t protecting staff as they should.

I’d want to know why they aren’t protecting patients as they should.

I’d want them to know that they are in breach of UK legislation .

And I’d want to look them in the eye and ask them to show compassion to the powerless: to staff, and patients.

Help us please.

Do whatever you can to counter the lies, and to help protect the NHS.

Thank-you.”

✾

‘A new campaign has launched demonstrating the importance of simple ventilation techniques to reduce the risks of catching COVID-19 this winter.’

�� (5 Nov 2021 ~ UK Department of Health and Social Care) New campaign to 'Stop COVID-19 hanging around' ➤

📖 Unravelling the connection between COVID-19 and Alzheimer’s disease: a comprehensive review

Mon, 08 Jan 2024 17:22:59 GMT

‘[COVID-19’s] ability to invade the central nervous system through the hematogenous and neural routes, besides attacking the respiratory system, has the potential to worsen cognitive decline in Alzheimer’s disease patients.

The severity of this issue must be highlighted.’

❦ ‘Alzheimer’s disease (AD) is acknowledged by the World Health Organisation (WHO) as a global public health concern.

AD is the primary cause of dementia and accounts for 50–70% of cases.

SARS-CoV-2 can damage the peripheral and the central nervous system (CNS) through both direct and indirect pathways, potentially leaving COVID-19 patients at higher risks for neurological difficulties, including depression, Parkinson’s disease, AD, etc., after recovering from severe symptoms.

Patients who recovered from severe COVID-19 infection are more likely to acquire stable neuropsychiatric and neurocognitive conditions like depression, obsessive-compulsive disorder, psychosis, Parkinson’s disease, and Alzheimer’s disease.

Severe systemic inflammation caused by SARS-CoV-2 is predicted to have long-term negative consequences, such as cognitive impairment.

Research has demonstrated that SARS-CoV-2-infected AD patients had a higher mortality rate. In a study from the Department of Neuroscience at the University of Madrid, 204 participants with Frontotemporal Dementia (FTD) and Alzheimer’s disease (AD) were enrolled.

According to the study, 15.2% of these individuals had COVID-19 infection, and sadly, 41.9% of those who had the virus died as a result of their illness.

In response to the impact of COVID-19 in 2020, governments worldwide acted promptly by implementing various public health measures.

During this period, people with cognitive impairments such as dementia or AD may have experienced greater stress and anxiety due to sudden changes in the environment and people’s behaviour.

It is also significantly harder for AD patients to comprehend and execute defensive measures such as wearing face masks and sanitising frequently.

❂

COVID-19 has generated a worldwide outbreak, resulting in a slew of issues for humans, particularly those suffering from Alzheimer’s disease.

Its ability to invade the central nervous system through the hematogenous and neural routes, besides attacking the respiratory system, has the potential to worsen cognitive decline in Alzheimer’s disease patients.

The severity of this issue must be highlighted.’

❂

�� (8 Jan 2024 ~ Frontiers in Aging Neuroscience) Unravelling the connection between COVID-19 and Alzheimer’s disease: a comprehensive review ➤

On testing: a question and answer

Sat, 06 Jan 2024 17:14:21 GMT

❦ Q . Why is it important for me to know if I have a COVID-19 infection?

❦ A . If you don’t recover well, it can help your doctor to know if you’ve had a COVID-19 infection – so that they can more effectively treat any of your on-going symptoms.

It also helps you to be conscious of the fact that contact with other people might hurt, permanently damage, or kill them.

➲ Few who self-test with an at-home rapid Lateral Flow Test (LFT) swab correctly or regularly enough – leading to false negatives , and a false idea of infection status .

In order to protect other people, it is advised that you begin testing daily after showing symptoms .

❂ As of January 2024 , SARS-CoV-2 infections may show as a positive result from between 2 and 7 days after symptoms have begun . *

* [ As of December 2024 , many symptomatic cases are now only showing as positive on LFTs/RATs on Day 6-7 with the JN.1/“Pirola” clan of 2024.]

❂ A negative result from a single self-test is not confirmation of negative-infection status.

❂

❦ Method :

➲ It is essential to swab the back of your throat as well as the back of your nose , underneath your tongue , inside your gums , and the insides of your cheeks for the most accurate results.

Five seconds of swabbing per site is recommended.

Whether you are using a series of at-home lateral flow tests or a PCR test to confirm a positive infection, it is also strongly advised that you swab routinely with LFT home-tests after your initial , short-term (acute) symptoms have gone away to help confirm your negative infectious status .

(This is sometimes referred to as “testing yourself out of an infection”.)

Several days of continuous negative tests may indicate that you are no longer infectious to others.

❂

➲ Please note that COVID-19 symptoms often vary as the virus changes and mutates.

➲ COVID-19 symptoms can often overlap with or mimic other respiratory and gastrointestinal diseases.

❂

More by... C19.Life

📖 Muscle abnormalities worsen after post-exertional malaise in long COVID

Thu, 04 Jan 2024 17:29:36 GMT

Post-exertional malaise (PEM) is a marked physical or mental fatigue and deterioration of symptoms occurring after physical , cognitive , social or emotional exertion that would have been tolerated previously.

Symptoms typically worsen 12 to 48 hours after such activities , and can last for days , weeks or months , making it difficult to manage or predict.

PEM is a hallmark symptom of myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS), and is commonly reported by people with Post-COVID-19 Syndrome (PCS/‘Long Covid’).

PEM can be mitigated by activity management , or ‘ pacing ’.

�� (4 Jan 2024 ~ Nature Communications) ‘Muscle abnormalities worsen after post-exertional malaise in long COVID’.

‘ A distinctive symptom of patients with long COVID is post-exertional malaise , which is associated with a worsening of fatigue- and pain-related symptoms after acute mental or physical exercise . ’

�� (4 Jan 2024 ~ News Medical Life Sciences) ‘Study identifies mitochondrial dysfunction as cause of long-COVID fatigue’.

❦ Scientific Media Article ~ ‘ Study identifies mitochondrial dysfunction as cause of long-COVID fatigue ’

By Amsterdam University Medical CenterNews / News Medical Life Sciences ( 4 Jan 2024 )

❦ ‘Researchers from Amsterdam UMC and Vrije Universiteit Amsterdam (VU) have discovered that the persistent fatigue in patients with long-COVID has a biological cause, namely mitochondria in muscle cells that produce less energy than in healthy patients.

25 long-COVID patients and 21 healthy control participants participated in the study. They were asked to cycle for fifteen minutes. This cycling test caused a long-term worsening of symptoms in people with long-COVID, called post-exertional malaise (PEM).

‘Extreme fatigue occurs after physical, cognitive, or emotional exertion beyond an unknown, individual threshold.’

The researchers looked at the blood and muscle tissue 1 week before the cycling test and 1 day after the test.

“We saw various abnormalities in the muscle tissue of the patients. At the cellular level, we saw that the mitochondria of the muscle, also known as the energy factories of the cell, function less well and that they produce less energy,” says Rob Wüst, Assistant Professor at Department of Human Movement Sciences at the VU University.

“So, the cause of the fatigue is really biological. The brain needs energy to think. Muscles need energy to move. This discovery means we can now start to research an appropriate treatment for those with long-COVID,” adds van Vugt.

One of the theories about long-COVID is that coronavirus particles may remain in the body of people who have had the coronavirus.

“We don’t see any indications of this in the muscles at the moment,” says Van Vugt.

The researchers also saw that the heart and lungs functioned well in the patients. This means that the long-lasting effect on patient’s fitness is not caused by abnormalities in the heart or lungs.

Exercising is not always good for patients with long-COVID.

“In concrete terms, we advise these patients to guard their physical limits and not to exceed them. Think of light exertion that does not lead to worsening of the complaints. Walking is good, or riding an electric bike, to maintain some physical condition. Keep in mind that every patient has a different limit,” says Brent Appelman, researcher at Amsterdam UMC.

“Because symptoms can worsen after physical exertion, some classic forms of rehabilitation and physiotherapy are counterproductive for the recovery of these patients,” van Vugt adds.

Although the majority of people infected with the SARS-CoV-2 virus recover within weeks, a subgroup, estimated to be around one in eight, will get long-COVID.

Symptoms in patients with long-COVID, post-acute sequelae or COVID or post-COVID syndrome (PCS) include severe cognitive problems (‘brain fog’), fatigue, exercise intolerance, autonomic dysregulation, postural orthostatic tachycardia syndrome (POTS), orthostatic intolerance, and worsening of symptoms after PEM. ’

�� (4 Jan 2024 ~ News Medical Life Sciences) ‘Study identifies mitochondrial dysfunction as cause of long-COVID fatigue’.

❂

‘ Viral infections can alter mitochondrial function , and multiple studies have shown that residual SARS-CoV-2 protein presence is associated with long COVID. ’

�� (4 Jan 2024 ~ Nature Communications) ‘Muscle abnormalities worsen after post-exertional malaise in long COVID’.

❦ Study ~ ‘ Muscle abnormalities worsen after post-exertional malaise in long COVID ’

By Appelman et al / Nature: Communications ( 4 Jan 2024 )

❦ ‘A subgroup of patients infected with SARS-CoV-2 remain symptomatic over three months after infection.

A distinctive symptom of patients with long COVID is post-exertional malaise, which is associated with a worsening of fatigue- and pain-related symptoms after acute mental or physical exercise, but its underlying pathophysiology is unclear.

With this longitudinal case-control study, we provide new insights into the pathophysiology of post-exertional malaise in patients with long COVID.

‘Local and systemic metabolic disturbances, severe exercise-induced myopathy, infiltration of amyloid-containing deposits, and immune cells in skeletal muscles of long COVID are key characteristics of post-exertional malaise.’

We show that skeletal muscle structure is associated with a lower exercise capacity in patients, and local and systemic metabolic disturbances, severe exercise-induced myopathy and tissue infiltration of amyloid-containing deposits in skeletal muscles of patients with long COVID worsen after induction of post-exertional malaise.

This study highlights novel pathways that help to understand the pathophysiology of post-exertional malaise in patients suffering from long COVID and other post-infectious diseases.’

Figure 1: ‘Lower exercise capacity in patients with long COVID.’

Figure 3: ‘Metabolic and mitochondrial dysfunction in long COVID patients worsens with post-exertional malaise.’

✾

�� (4 Jan 2024 ~ Nature Communications) Muscle abnormalities worsen after post-exertional malaise in long COVID ➤

�� (4 Jan 2024 ~ Amsterdam University Medical Center / News Medical Life Sciences) Study identifies mitochondrial dysfunction as cause of long-COVID fatigue ➤

❦ How to commit hara-kiri ( and knock down a scarecrow) in the field of academia

A little over a year after Appelman et al ’s Nature paper on mytochondrial dysfunction and PEM, Brigitte Ranque (with friends) decides to publish a rebuttal – for they are in the business of GET and CBT , and accurate science hurts their bottom line.

A ‘ straw man ’ is dispatched to Nature ...

�� ( 11 Feb 2025 ~ Nature Communications) ‘Reply: Muscle abnormalities in Long COVID ’ [ Ranque et al ] ➤

‘The biology of the “kickbacks” (post exertional malaise, PEM) after activity experienced by people with the post-COVID-19 condition (long COVID) is debated. Some specialists believe it is a result of a protective brain response, and others that it is the result of pathophysiology in the muscle itself. Appelman and colleagues report on muscle damage following a maximal effort physical exercise test in patients with PEM with the COVID-19 condition, and these results are interpreted as showing that exercise damages the tissues of people with PEM and should therefore be avoided. However, we believe the data reported do not support this interpretation, as the patients were substantially deconditioned; the physical activity was extreme and biological changes would be expected in anyone; and there were no control patients with a post-COVID-19 condition without PEM. The implications of erroneous interpretation of these data could result in patients fearing that PEM causes physical damage and consequently avoiding approaches to rehabilitation that could help them...’

Etc, etc, etc.

❦ On pressing on with good researchers’ time

The problem with disinformation is that it takes an awful lot of time, and energy and effort, to prove its harm...

(On Ranque and colleagues’ “deconditioning” argument, note the 2024 Lancet study * regarding young (median age 18) US marines.)

* �� (23 Oct 2024 ~ The Lancet: Regional Health/America) Clinical and functional assessment of SARS-CoV-2 sequelae among young marines – a panel study ➤

�� ( 11 Feb 2025 ~ Nature Communications) ‘Reply: Muscle abnormalities in Long COVID ’ [ Appelman et al ] ➤

‘We thank Ranque et al. for their interest in our recent work and alternative interpretation of our data. We refute that our findings are due to deconditioning, as Long COVID-related skeletal muscle differ fundamentally from those caused by deconditioning. We demonstrated significant physiological differences in Long COVID patients with post-exertional malaise (PEM) compared to healthy controls, even at matched physical activity levels. PEM encompasses a variety of symptoms and not only muscle soreness. Our study did not address the efficacy of exercise training, and we reject misinterpretations that all forms of exercise cause PEM. We advocate further research to define safe exercise thresholds and improve the understanding of PEM.

Ranque et al. state that “everyone can experience severe muscle pain when returning to intense exercise after periods of a few weeks of rest”. Every participant experienced maximal exercise, healthy participants with low fitness also participated, and a proportion of Long COVID patients still possessed fitness levels >50th percentile for their respective sex and age, despite all patients experiencing PEM. Despite several controls having a VO₂ max similar to patients, none reported PEM symptoms...’

Etc.

✾

More... Post-Exertional Malaise (PEM)

More... PASC (PCS / ‘Long Covid’)