Immunity

on immunity

“People do become very worried if you compare COVID-19 to HIV, but actually HIV has good treatment and life expectancy now.”

Dr. Noor Bari, Emergency Medicine (2023)

❦ on three scenarios

“COVID-19 is fighting back by generally depressing the whole adaptive immune system.


We are showing narrow resilience to COVID reinfections due to adapting – but we are becoming more vulnerable in general to infections of all kinds.

➲ Worst case scenario


A single infection causes on-going and progressive immunodeficiency.

➲ Best case scenario


A single infection causes temporary immunosuppression, and we suppress COVID transmission enough to allow recovery.

➲ Most likely scenario, medium-term


Immunosuppression that becomes continuous and possibly progressive due to reinfections.

Reduced immune function after a viral infection is not unusual.


Many viruses do this.


The concerning issue is the length and breadth of the immune system dysfunction, coupled with emerging evidence of other pathogens taking advantage.”

Dr. Noor Bari, Emergency Medicine (2023)

❦ Immunosuppression ~ Suppression of the immune system and its ability to fight infection.


❦ Immunodeficiency ~ A state in which the immune system’s ability to fight infectious diseases and cancer is compromised, or entirely absent.

❦ on repeated exposure

‘Repeated exposure to a virus such as SARS-CoV-2 will fast-track more people into immunosenescence at ever-earlier ages, with potentially serious repercussions for their health and longevity.’

The John Snow Project (2023)

❦ Immunosenescence ~ The gradual deterioration of the immune system, normally brought on by natural age advancement.


Immunosenescence is closely related to the development of infections, autoimmune diseases, and malignant tumors.

❦ on lymphocytopenia

The most common causes of acquired lymphocytopenia include:


➲ Protein-energy undernutrition.

➲ HIV infection.

➲ COVID-19.

➲ Certain other viral infections.


Patients with HIV infection routinely have lymphocytopenia, which arises from destruction of CD4+ T cells infected with the HIV virus.


➲ Patients with COVID-19 also frequently have lymphocytopenia (35% to 83% of patients).


➲ Patients have recurrent viral, bacterial, fungal, or parasitic infections.

Merck Manual ➲ (2023)

❦ on the hygiene hypothesis, and pathogenic viruses

‘The hygiene hypothesis is the idea that the immune system needs to be “trained” during childhood to properly develop immune tolerance to microbes, but it specifically refers to bacteria, protozoans and helminths, most of which are normally beneficial, neutral or not significantly harmful to humans.


It does not advocate repeated exposure to viruses, especially highly pathogenic ones.’

The John Snow Project (2023)

❦ immunity ~ further reading

On vaccine-induced herd immunity, widespread booster roll-outs... and the UK

by Cat in the Hat • 22 Nov, 2023
❦ Chris Whitty, from the Covid Inquiry: “The one situation... that you would ever aim to achieve herd immunity is by vaccination . That is the only situation that is a rational policy response.” And yet... the UK is no longer offering vaccines to the vast majority of its working-age population. According to the JCVI member Dr Adam Finn, the UK’s strategy going forward is that: “... most under 65’s will now end up boosting their immunity not through vaccination, but through catching Covid many times .” ➲ (24 Sep 2023 ~ BBC) What you need to know about Covid as new variant rises ➤ Let me translate: The stated aim is to get infected over and over and over again... to protect against being infected over and over and over again! How does this make any sense at all? The government has decided that it is not good “value for money” to actually give the boosters out – even for the age groups who have already had Covid vaccine doses purchased for them (for example, the 50-65 year olds) – so millions of doses [8.5 million] are now destined to be binned, rather than being used. ➲ ‘COVID VACCINE: COST EFFECTIVENESS ASSESSMENT. For the first time ever, the UK government has used a ‘bespoke, non-standard cost-effectiveness assessment’ to decide who would be eligible for the Covid booster this Autumn. In this thread, I explore how this assessment was undertaken…’ ➤ Meanwhile, in many other countries, the booster is open to anyone who wants it . No strict eligibility criteria. Just step forward and get protected. Let’s take a look at a few: 1. THE USA : Covid booster available to EVERYONE aged 6 months and older. The CDC (USA’s Centers for Disease Control ) recommends that everyone ages 6 months and upwards get the updated COVID-19 booster to protect against serious illness. The new vaccine targets the most common circulating variants, and should be available later this week. The full details are here ➤ . 2. CANADA : Covid booster available to EVERYONE aged 6 months and older. Full details are here ➤ . 3. FRANCE : Covid booster available to EVERYONE. Full details are here ➤ . 4. BELGIUM : Covid booster available to EVERYONE. Full details are here ➤ . 5. JAPAN : Covid booster available to EVERYONE aged 6 months and older. Full details are here ➤ . Why is the UK falling so far out of step with so many other countries on their Covid vaccine strategy? How can they justify binning millions of purchased vaccine doses when there are many people who would gladly take them? ➲ ‘So what’s going to happen to the millions of purchased doses which now won’t be used? Well, here’s the real kicker... it seems they’re destined for the bin. A number of alternative uses have been considered, but the conclusion is: “THESE DOSES HAVE NO FEASIBLE ALTERNATIVE USE”. ’ ➤ If the UK government won’t fund deployment of the Covid jab to EVERYONE (as so many other countries do), then why isn’t there at least an option to buy it privately? This model already exists with the flu jab – why is there not the same option for Covid? © 2023 Cat in the Hat ➲

On brazen idiocy, propaganda, and the throwing of under-65s off a white cliff

by Dr. Adam Finn, Professor of Paediatrics, University of Bristol / Jim Reed, BBC • 24 Sept, 2023
❦ ‘The emergence of [new SARS-CoV-2 Variant of Interest] BA.2.86 meant a decision was made to bring forward the autumn Covid booster to better protect the most vulnerable this winter. But the new jabs are only available to people over 65 years old – it was the over-50s last year – and those with certain health conditions. That is a tactical decision , says Dr. Adam Finn, Professor of Paediatrics at the University of Bristol. He explained: “When younger people who’ve already had infections and vaccines get Covid [again], they get a cold and a cough and might be off work for a few days. There’s no real value in investing a lot of time and effort immunising them again when there are so many other things for the Health Service to be doing.” [ ❦ Note : Can a 62-year-old be defined as a ‘ younger person ’? Yes, at a pinch, if Mr. Finn compares them to a 78-year-old. What age-group do these ‘ younger people ’ belong to who don’t need vaccinating, and who instead need to be continually reinfected with a highly pathogenic Biohazard-Level 3 virus? Could it be a 32-year-old man or woman hoping to have a baby ? Or the 0 to 19-year-olds , who are the academic professor’s strong suit? ] ‘The reality is then that most under-65s will now end up boosting their immunity not through vaccination , but through catching Covid many times . In general, Prof Finn says each new infection should feel milder with the length of time you are sick reduced [sic] . “Each time you catch it, your immunity gets stronger and broader ,” he adds. ’ ❂ [ Note : This is simply not true, and is staggeringly dangerous. ] ❂ 📖 (24 Sep 2023 ~ Jim Reed, Health Reporter / BBC online) What you need to know about Covid as new variant [BA.2.86] rises ➤ © 2023 BBC .

📖 On Lymphocytopenia

by Merck and Co. • 16 Sept, 2023
❦ ‘The most common causes of acquired lymphocytopenia include: ➲ Protein-energy undernutrition. ➲ HIV infection. ➲ COVID-19 . ➲ Certain other viral infections. Patients with HIV infection routinely have lymphocytopenia, which arises from destruction of CD4+ T cells infected with the HIV virus. Patients with COVID-19 also frequently have lymphocytopenia ( 35% to 83% of patients ) . Lower lymphocyte counts portend a poor prognosis and an increased likelihood of requiring ICU admission and of dying from the disease. The cause of the lymphocytopenia is not completely understood, but COVID-19 can directly infect lymphocytes, and a cytokine-related apoptosis of the cells is likely. ➲ Lymphocytopenia is most often due to AIDS , and recently COVID-19 , or undernutrition, but it also may be inherited or caused by various infections, drugs, or autoimmune disorders. ➲ Patients have recurrent viral , bacterial , fungal , or parasitic infections .’ ❂ 📖 (Accessed 16 Sep 2023 ~ Merck & Co.) Entry for 'Lymphocytopenia' in Merck Manual ➤ © 2023 Merck & Co .

On immune systems, and chewing on the leftovers

by Dr. Noor Bari, Emergency Medicine • 27 Aug, 2023
❦ 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. © 2023 Dr. Noor Bari . ➲

📖 The immunology of long COVID

by Altmann et al / Nature • 11 Jul, 2023
❦ ‘Long COVID is the patient-coined term for the disease entity whereby persistent symptoms ensue in a significant proportion of those who have had COVID-19, whether asymptomatic, mild or severe. The disease burden spans from mild symptoms to profound disability, the scale making this a huge, new healthcare challenge. Long COVID will likely be stratified into several more or less discrete entities with potentially distinct pathogenic pathways. The evolving symptom list is extensive, multi-organ, multisystem and relapsing–remitting, including fatigue, breathlessness, neurocognitive effects and dysautonomia. A range of radiological abnormalities in the olfactory bulb, brain, heart, lung and other sites have been observed in individuals with Long COVID. Some body sites indicate the presence of microclots; these and other blood markers of hypercoagulation implicate a likely role of endothelial activation and clotting abnormalities. Diverse auto-antibody (AAB) specificities have been found, as yet without a clear consensus or correlation with symptom clusters. There is support for a role of persistent SARS-CoV-2 reservoirs and/or an effect of Epstein-Barr virus reactivation, and evidence from immune subset changes for broad immune perturbation. The oncoming burden of Long COVID faced by patients, healthcare providers, governments and economies is so large as to be unfathomable, which is possibly why minimal high-level planning is currently allocated to it.’ ❂ 📖 (11 July 2023 ~ Nature Reviews: Immunology) The immunology of long COVID ➤ © 2023 Altmann et al / Nature.

📖 SARS-CoV-2 and “Textbook” Immunity

by The John Snow Project • 05 May, 2023
❦ Prior to 2020, there were four endemic human coronaviruses – OC43, NL-63, 229E, and HKU1 – which were known to cause 10 to 15 percent of common colds – or the ‘Common Cold Coronaviruses’ (CCCs).  From at least the 1970s, we’ve known that infection with these coronaviruses does not lead to lasting protection from reinfection – this is textbook knowledge. CCCs are not just colds – they can cause severe pneumonias, and exhibit a risk profile very similar to SARS-CoV-2 with age. If reinfection really did strengthen immunity against CCCs, then older people would be the least affected – because they would have been regularly infected with diverse variants of these viruses in their past. But that is not the case – and SARS-CoV-2 is not a CCC. SARS-CoV-2 has a wide array of accessory proteins that silence and disrupt our normal immune responses. As we get older, our immune systems start to lose their effectiveness – and we become more susceptible to disease. This process is called immunosenescence . Repeated exposure to a virus like SARS-CoV-2 is fast-tracking more people into immunosenescence at ever-earlier ages, with potentially serious repercussions for their health and longevity. SARS-CoV-2 is a particularly nasty virus that can also trigger the hyperactivation of our own immune systems to cause severe disease. Infection by SARS-CoV-2 has been shown to lead to an increase in autoantibodies and autoimmune disease. Approximately 25 percent of people who develop an autoimmune disease will experience multiple autoimmune syndrome, and will risk a cascade of autoimmune conditions. SARS-CoV-2, like its 2002 predecessor SARS-CoV-1, is both a respiratory and a systemic virus, with an extremely broad cell-type and tissue-tropism covering nearly the whole body. Its ability to infect and do damage to lungs, hearts, kidneys, cardiovascular systems and brains is particularly well-documented. If each subsequent infection results in additional internal organ and immune-system damage, then at some point the damage accumulated – together with the accelerated immune-system aging and normal aging processes – can reasonably be expected to outweigh the protective benefits of immunity developed from previous infections. SARS-CoV-2 reinfects more frequently than influenza or the common cold, infects a wider range of organs, does more damage and seems capable of persisting in a range of organs. So if SARS-CoV-2 behaves like a textbook virus – but does more damage more quickly and more regularly – at what point does the body reach its tipping point? ❂ There are two versions of this article: a 7-minute read in simplified language ; and the full editorial version complete with references, which is an 18-minute-read and aimed towards the medical and scientific communities . ❦ 7-minute primer ~ ‘SARS-CoV-2 and “Textbook” Immunity’ ➤ ❦ Full 18-minute editorial ~ ‘SARS-CoV-2 and “Textbook” Immunity’ ➤ ❂ 📖 (5 May 2023 ~ The John Snow Project) SARS-CoV-2 and "Textbook" Immunity ➤ © 2023 The John Snow Project.

📖 Fungal infection profile in critically ill COVID-19 patients: a prospective study at a large teaching hospital in a middle-income country

by Negm et al / BMC Infectious Diseases • 23 Apr, 2023
❦ Critically ill COVID-19 patients are highly susceptible to opportunistic fungal infection due to many factors, including virus-induced immune dysregulation , host-related comorbidities, overuse and misuse of antibiotics or corticosteroids, immune modulator drugs, and the emergencies caused by the pandemic. Fungal coinfection is a common complication of critically ill COVID-19 patients admitted to the ICU. Candidiasis , aspergillosis , and mucormycosis are the most common COVID-19-associated fungal infections and have a great impact on mortality rates . ❂ 📖 (18 Apr 2023 ~ BMC Infectious Diseases) Fungal infection profile in critically ill COVID-19 patients: a prospective study at a large teaching hospital in a middle-income country ➤ © 2023 Negm et al / BMC Infectious Diseases.

📖 Status of major hemostatic components in the setting of COVID-19: the effect on endothelium, platelets, coagulation factors, fibrinolytic system, and complement

by Sayyadi et al / Annals of Hematology • 19 Apr, 2023
❦ ‘COVID-19 patients have a hypercoagulability state, and thrombosis is a life-threatening complication of them.’ ✻ Hypercoagulability , also known as thrombophilia , is a condition in which there is an abnormally increased tendency towards blood clotting . ‘From the early days of the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) outbreak to the present, clinical and basic studies have indicated that coronavirus disease 2019 (COVID-19) may be associated with coagulopathy ( CAC ), which is involved in its related morbidity and mortality. Deep vein thrombosis ( DVT ) and pulmonary embolism ( PE ) are common in COVID-19 patients and are remarkably high in the intensive care unit (ICU)–admitted patients. CAC can lead to the formation of circulating microthrombi and macrothrombi which can involve multiple sites, including the lungs , brain , heart , and visceral organs like kidneys and spleen . There is a close relationship between the immune system and coagulation. The components of the hemostatic system play a role in the body’s immunity, and the activation of the immune system strongly influences the hemostatic system. Abnormal activation of the immune system may promote the growth of pathologies associated with thrombosis. COVID-19 is accompanied by an immune-cell hyperactivation and excessive production of proinflammatory cytokines , known as “ cytokine storm ”. CAC is theorized to result from dysregulated interactions between the immune and coagulation systems .’ ❂ 📖 (19 Apr 2023 ~ Annals of Hematology) Status of major hemostatic components in the setting of COVID-19: the effect on endothelium, platelets, coagulation factors, fibrinolytic system, and complement ➤ © 2023 Annals of Hematology .

📖 Long-term risk of herpes zoster [shingles] following COVID-19: A retrospective cohort study of 2,442,686 patients

by Chen et al / Journal of Medical Virology • 18 Apr, 2023
❦ 'The risk of herpes zoster (HZ) ( Shingles ) remained significantly [+60%] higher in patients with COVID-19 compared with those without COVID-19. The higher risk of HZ in the COVID-19 cohort compared with that in the non-COVID-19 cohort remained consistent across subgroup analyses regardless of vaccine status, age, or sex. The risk of HZ within a 12-month follow-up period was significantly higher in patients who had recovered from COVID-19 compared with that in the control group. ❂ 📖 (18 Apr 2023 ~ Journal of Medical Virology) Long-term risk of herpes zoster following COVID-19: A retrospective cohort study of 2 442 686 patients ➤ © 2023 Journal of Medical Virology.

📖 High risk of autoimmune diseases after COVID-19

by Sharma & Jagadeesh / Nature Reviews: Rheumatology • 12 Apr, 2023
❦ The full picture of post-COVID-19 autoimmune diseases and their prevalence is lacking despite numerous case reports and small series. Two studies that use large cohorts now highlight that SARS-CoV-2 infection is linked to a substantially increased risk of developing a diverse spectrum of new-onset autoimmune diseases . The reports by Chang et al and Tesch et al provide a comprehensive overview of diverse new-onset autoimmune conditions after COVID-19. In addition, an earlier preprint of a retrospective matched cohort analysis using data from the Clinical Practice Research Datalink Aurum database of 458,147 SARS-CoV-2-infected and 1,818,929 uninfected adults across England between 31 January 2020 and 30 June 2021 reported that the incidence of type 1 diabetes mellitus , inflammatory bowel disease and psoriasis are significantly associated with SARS-CoV-2 infection. Some of the earliest evidence that SARS-CoV-2 infection leads to dysregulated immune responses came from paediatric patients who presented with multisystem inflammatory syndrome in children (MIS-C) , which, as the name indicates, involves diffuse organ system involvement and a clinical spectrum that overlaps with other hyperinflammatory syndromes , such as Kawasaki disease , toxic-shock syndrome , and macrophage activation syndrome . Since the start of the pandemic, many researchers have also reported isolated cases of adults with various post-COVID-19 autoimmune conditions. ❂ 📖 (12 Apr 2023 ~ Nature Reviews: Rheumatology) High risk of autoimmune diseases after COVID-19 ➤ © 2023 Sharma & Jagadeesh / Nature.

📖 SARS-CoV-2 infection of thymus induces loss of function that correlates with disease severity

by Rosichini et al / Journal of Allergy and Clinical Immunology • 07 Feb, 2023
❦ Lymphopenia , particularly when restricted to the T-cell compartment, has been described as one of the major clinical hallmarks in patients with coronavirus disease 2019 ( COVID-19 ) and proposed as an indicator of disease severity. Although several mechanisms fostering COVID-19-related lymphopenia have been described, including cell apoptosis and tissue homing, the underlying causes of the decline in T-cell count and function are still not completely understood. Patients with COVID-19 had reduced thymic function that was inversely associated with the severity of the disease. Our data demonstrate that the human thymus is a target of SARS-CoV-2 and thymic function is altered following infection . Note: Lymphopenia (also called lymphocytopenia) is a disorder in which your blood doesn't have enough white blood cells called lymphocytes. Lymphocytes play a protective role in your immune system. ❂ 📖 (7 Feb 2023 ~ Journal of Allergy and Clinical Immunology) SARS-CoV-2 infection of thymus induces loss of function that correlates with disease severity ➤ © 2023 Rosichini e t al / Journal of Allergy and Clinical Immunology.

📖 Children's immune systems do not develop 'adaptive memory' to protect against second-time SARS-CoV-2 infection

by Emily Henderson / Medical Life Sciences • 26 Jan, 2023
❦ ‘Children have largely avoided severe COVID-19 symptoms because they have a strong initial ‘innate’ immune reaction that quickly defeats the virus. But unlike those of adults, children’s immune systems don’t remember the virus and don’t adapt, so when they’re next exposed to SARS-CoV-2, their body still treats it as a new threat. “Because children haven’t been exposed to many viruses, their immune system is still ‘naive’. And because they don't develop memory T cells, they are at risk of getting sick when they become reinfected. With each new infectious episode as they get older, there is a risk of their T cells becoming ‘exhausted’ and ineffective, like the T cells in older people. 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,” says Professor Tri Phan.’ ❂ 📖 (26 Jan 2023 ~ Medical Life Sciences) Children's immune systems do not develop 'adaptive' memory to protect against second-time SARS-CoV-2 infection ➤ 📖 (January 2023 ~ Clinical Immunology) Tracking the clonal dynamics of SARS-CoV-2-specific T cells in children and adults with mild/asymptomatic COVID-19 ➤ © 2023 Emily Henderson / Medical Life Sciences.

📖 New insights into deadly fungal invasion in people with compromised immune systems

by Emily Henderson / News Medical Life Sciences • 12 Jan, 2023
❦ Fungi such as Aspergillus are so common in our surroundings that we breathe in hundreds to thousands of spores every day. In healthy people, fungi typically pose no threat, but they can cause deadly infections in those with compromised immune systems. However, it is increasingly recognized that viral infections such as influenza or SARS-CoV-2 can increase the risk of invasive Aspergillus infections even in healthy people. ❂ 📖 (12 Jan 2023 ~ News-Medical.Net) New insights into deadly fungal invasion in people with compromised immune systems ➤ © 2023 Emily Henderson / News Medical Life Sciences.

📖 Immune systems seriously weakened by COVID

by Terry Pender / Waterloo Region Record • 20 Dec, 2022
❦ Evolving research says COVID leaves many people at heightened risk for other infections. SARS-CoV-2 depletes the body’s supply of T-cells, * leaving young and old alike vulnerable to secondary infections. * (T-cells are the ‘front-line soldiers’ of the immune system, and the number of T-cells typically increases when the body is fighting off an infection.) “Individuals who are infected with COVID have many fewer T-cells – that’s a problem for us, because T-cells are a really important part of our immune system that helps defend us against infection.” But at least three studies show ✢ that COVID kills off a significant number of the body’s T-cells – so even when someone recovers from COVID, they are at a heightened risk for other viral, bacterial and fungal infections. “With the loss of these T-cells, we are now more vulnerable to all of these other infections, other viruses, other bacteria.” COVID-19 sparks what is called ‘programmed cell death’ among T-cells. Cells in the human body do this naturally as they age, but COVID-19 causes healthy T-cells to die that would otherwise be available to fight off infections. Many people who have had COVID brush it off, saying it was no worse than a bad case of the flu. What they don’t know is that they are more vulnerable to secondary infections that may cause them to seek help at a hospital emergency ward. ❂ ✢ 📖 (11 Jan 2023 ~ Nature Reviews / Immunology) Innate immune evasion strategies of SARS-CoV-2 ➤ 📖 (13 Jan 2023 ~ Preprint) Structure-based discovery of inhibitors of the SARS-CoV-2 Nsp14 N7-methyltransferase ➤ 📖 20 Apr 2021 ~ Nature / Cell Death & Differentiation) SARS-CoV-2 spike protein dictates syncytium-mediated lymphocyte elimination ➤ ❂ 📖 (20 Dec 2022 ~ Waterloo Region Record) Immune systems seriously weakened by COVID ➤ © 2022 Terry Pender / Waterloo Region Record.

📖 COVID-19 disease and immune dysregulation

by Davitt et al / Best Practice & Research Clinical Haematology • 06 Dec, 2022
❦ While COVID-19 was originally characterized as hyperinflammatory in its pathophysiology, emerging evidence demonstrates the possibility of a strongly immunosuppressive phenotype in more critical disease states. While immune activation from neutrophils and complement may contribute to inflammatory damage in the lungs, decreased antiviral responses, dysregulated macrophages and dendritic cells, and severe lymphopenia contribute to a suppressed state in which viral replication and secondary infections are prone. ❂ 📖 (6 Dec 2022 ~ Best Practice & Research Clinical Haematology) COVID-19 disease and immune dysregulation ➤ © 2022 Davitt et al / Best Practice & Research Clinical Haematology.

On post-COVID infections, immunodeficient patients and multi-drug-resistant diseases

by Dr. Noor Bari, Emergency Medicine • 10 Nov, 2022
❦ This morning someone said to me: — “I just can’t shake this... first a chest infection, and now a urine infection...” Someone else I know (very close) has had three eye infections post-COVID. Another has had a deterioration in their fertility, as compared to their baseline pre- and post-COVID. Measured. It’s almost as if the stuff in the science papers is real. None of them have twigged that COVID might have toasted them yet either. They are all heading into this next wave with no idea how dangerous it might be to abuse their already struggling immune system like this. You know what’s coming next... Multi-drug-resistant bacteria. Many are already here, but this is going to get really out of control. Trying to treat infections in immunodeficient patients is a great way to make loads of drug-resistant bacteria and viruses. ❂ 📖 (24 May 2023 ~ Current Microbiology) Interaction Between SARS-CoV-2 and Pathogenic Bacteria ➤ 📖 (18 Apr 2023 ~ BMC Infectious Diseases) Fungal infection profile in critically ill COVID-19 patients: a prospective study at a large teaching hospital in a middle-income country ➤ 📖 (29 Mar 2023 ~ Journal of Fungi) Fungal-Bacterial Co-Infections and Super-Infections among Hospitalized COVID-19 Patients: A Systematic Review ➤ 📖 (30 Sep 2021 ~ Insider) Drug-resistant infections in the US have risen sharply during the pandemic, and experts warn it's getting worse as COVID patients overwhelm hospital resources ➤ © 2022 Dr. Noor Bari, Emergency Medicine ➲

On immunological dysfunction and post-COVID infections

by Dr. Noor Bari, Emergency Medicine • 30 Oct, 2022
❦ COVID-19 is fighting back by generally depressing the whole adaptive immune system. We are showing narrow resilience to COVID reinfections due to adapting – but we are becoming more vulnerable in general to infections of all kinds. ❦ Worst case scenario: a single infection causes on-going and progressive immunodeficiency . ❦ Best case scenario: a single infection causes temporary immunosuppression , and we suppress COVID transmission enough to allow recovery. ❦ Most likely scenario, medium-term: immunosuppression that becomes continuous and possibly progressive due to reinfections. Reduced immune function after a viral infection is not unusual. Many viruses do this. The concerning issue is the length and breadth of the immune system dysfunction, coupled with emerging evidence of other pathogens taking advantage. ❂ ❦ Immunosuppression ~ Suppression of the immune system and its ability to fight infection. ❦ Immunodeficiency ~ A state in which the immune system's ability to fight infectious diseases and cancer is compromised, or entirely absent. ❂ 📖 (13 Jan 2022 ~ Nature: Immunology) Immunological dysfunction persists for 8 months following initial mild-to-moderate SARS-CoV-2 infection ➤ © 2022 Dr. Noor Bari, Emergency Medicine ➲

📖 When COVID-19 or flu viruses kill, they often have an accomplice – bacterial infections

by Hayley Muendlein / The Conversation • 17 Aug, 2022
❦ The 1918 influenza pandemic resulted in the loss of over 3% of the world’s population – at least 50 million people. But it wasn’t the flu virus that caused the majority of these deaths. An analysis of lung samples collected during that flu pandemic indicated that most of the deaths were likely due to bacterial pneumonia , which ran rampant in the absence of antibiotics. Even in more recent history, like the 1957 H2N2 and 2009 H1N1 flu pandemics , nearly 18% of patients with viral pneumonia had additional bacterial infections that increased their risk of death. And the COVID-19 pandemic is no different. ❂  📖 (17 Aug 2022 ~ The Conversation) When COVID-19 or flu viruses kill, they often have an accomplice – bacterial infections ➤ © 2022 Hayley Muendlein / The Conversation.

On bat-like immune systems, and ‘living with the virus’

by Dr. Noor Bari, Emergency Medicine • 21 Jul, 2022
❦ So, we want to ‘live with the virus’. Is there any evidence of this occurring successfully anywhere? Yes! In bats... and it has taken 64 million years of evolution ✢ to get there. 📖 (20 Jan 2021 ~ Nature) Lessons from the host defences of bats, a unique viral reservoir ➤ To ‘live with the virus’, bats have better host defences – they don’t overdo inflammation, and they can get rid of toxic compounds and deal with reactive oxygen species much better than humans. They literally live with the virus . For humans to ‘live with the virus’, we would need to have similar mechanisms to permit SARS-CoV-2 to be part of our biome – without causing all of the autoimmune disease and other damage. We would have to have fundamentally different biochemistry and immune systems. We can mimic this using therapeutics to some extent, and this may help us treat Long COVID. However, I don’t think that we will naturally become resilient to SARS-CoV-2 for a very long time. What I’m trying to say is that mass-infecting this generation of children is unlikely to result in them developing a bat-like immune system within their lifetimes. It’s ridiculous that the attempt was ever made. I genuinely think that putting ventilation upgrades into every building and wearing good-quality masks will be easier than building a genetically modified SARS-resistant human. I keep trying to give you the easy way out! The coronavirus is moving into our bodies and is attempting to stay there, just like it does in bats. The problem is that our bodies try to fight it. We fight it well enough to reduce detectable virus-shedding on our breath, but there is evidence (persistent spike RNA) that the virus is hiding somewhere else in our body anyway. So our bodies keep fighting it. The collateral damage is the problem. What are our choices? 1. Figure out how to change human physiology so that we don’t burn ourselves out fighting an elusive and persistent enemy. 2. Or figure out how we can stop transmission. The second is easier, and economically sound. The ability to completely clear coronavirus is also a potential goal – but again, therapeutics will be needed because we have places where, if the immune system is left to do it, it causes damage – and coronavirus has many tricks to help it hide from detection. Needless to say, coronavirus can evolve a lot faster than we can, so we need to use our brain cells in a different way to fight COVID-19. Instead of using microglia, we need to think ...

📖 Coronavirus Deranges the Immune System in Complex and Deadly Ways

by Liz Szabo / KFF Health News • 04 Mar, 2021
❦ While all viruses find ways to evade the body’s defenses, a growing field of research suggests that the coronavirus unhinges the immune system more profoundly than previously realized. Some Covid survivors have developed serious autoimmune diseases, which occur when an overactive immune system attacks the patient, rather than the virus. Doctors in Italy first noticed a pattern in March 2020, when several Covid patients developed Guillain-Barré syndrome, in which the immune systems attacks nerves throughout the body, causing muscle weakness or paralysis. As the pandemic has surged around the world, doctors have diagnosed patients with rare, immune-related bleeding disorders. Other patients have developed the opposite problem, suffering blood clots that can lead to stroke. All these conditions can be triggered by autoantibodies – rogue antibodies that target the patient’s own proteins and cells. ❂ 📖 (4 Mar 2021 ~ KFF Health News) Coronavirus Deranges the Immune System in Complex and Deadly Ways ➤ © 2021 Liz Szabo / KFF Health News.

C-19 Blog:

immunity

On vaccine-induced herd immunity, widespread booster roll-outs... and the UK

by Cat in the Hat • 22 Nov, 2023
❦ Chris Whitty, from the Covid Inquiry: “The one situation... that you would ever aim to achieve herd immunity is by vaccination . That is the only situation that is a rational policy response.” And yet... the UK is no longer offering vaccines to the vast majority of its working-age population. According to the JCVI member Dr Adam Finn, the UK’s strategy going forward is that: “... most under 65’s will now end up boosting their immunity not through vaccination, but through catching Covid many times .” ➲ (24 Sep 2023 ~ BBC) What you need to know about Covid as new variant rises ➤ Let me translate: The stated aim is to get infected over and over and over again... to protect against being infected over and over and over again! How does this make any sense at all? The government has decided that it is not good “value for money” to actually give the boosters out – even for the age groups who have already had Covid vaccine doses purchased for them (for example, the 50-65 year olds) – so millions of doses [8.5 million] are now destined to be binned, rather than being used. ➲ ‘COVID VACCINE: COST EFFECTIVENESS ASSESSMENT. For the first time ever, the UK government has used a ‘bespoke, non-standard cost-effectiveness assessment’ to decide who would be eligible for the Covid booster this Autumn. In this thread, I explore how this assessment was undertaken…’ ➤ Meanwhile, in many other countries, the booster is open to anyone who wants it . No strict eligibility criteria. Just step forward and get protected. Let’s take a look at a few: 1. THE USA : Covid booster available to EVERYONE aged 6 months and older. The CDC (USA’s Centers for Disease Control ) recommends that everyone ages 6 months and upwards get the updated COVID-19 booster to protect against serious illness. The new vaccine targets the most common circulating variants, and should be available later this week. The full details are here ➤ . 2. CANADA : Covid booster available to EVERYONE aged 6 months and older. Full details are here ➤ . 3. FRANCE : Covid booster available to EVERYONE. Full details are here ➤ . 4. BELGIUM : Covid booster available to EVERYONE. Full details are here ➤ . 5. JAPAN : Covid booster available to EVERYONE aged 6 months and older. Full details are here ➤ . Why is the UK falling so far out of step with so many other countries on their Covid vaccine strategy? How can they justify binning millions of purchased vaccine doses when there are many people who would gladly take them? ➲ ‘So what’s going to happen to the millions of purchased doses which now won’t be used? Well, here’s the real kicker... it seems they’re destined for the bin. A number of alternative uses have been considered, but the conclusion is: “THESE DOSES HAVE NO FEASIBLE ALTERNATIVE USE”. ’ ➤ If the UK government won’t fund deployment of the Covid jab to EVERYONE (as so many other countries do), then why isn’t there at least an option to buy it privately? This model already exists with the flu jab – why is there not the same option for Covid? © 2023 Cat in the Hat ➲

On brazen idiocy, propaganda, and the throwing of under-65s off a white cliff

by Dr. Adam Finn, Professor of Paediatrics, University of Bristol / Jim Reed, BBC • 24 Sept, 2023
❦ ‘The emergence of [new SARS-CoV-2 Variant of Interest] BA.2.86 meant a decision was made to bring forward the autumn Covid booster to better protect the most vulnerable this winter. But the new jabs are only available to people over 65 years old – it was the over-50s last year – and those with certain health conditions. That is a tactical decision , says Dr. Adam Finn, Professor of Paediatrics at the University of Bristol. He explained: “When younger people who’ve already had infections and vaccines get Covid [again], they get a cold and a cough and might be off work for a few days. There’s no real value in investing a lot of time and effort immunising them again when there are so many other things for the Health Service to be doing.” [ ❦ Note : Can a 62-year-old be defined as a ‘ younger person ’? Yes, at a pinch, if Mr. Finn compares them to a 78-year-old. What age-group do these ‘ younger people ’ belong to who don’t need vaccinating, and who instead need to be continually reinfected with a highly pathogenic Biohazard-Level 3 virus? Could it be a 32-year-old man or woman hoping to have a baby ? Or the 0 to 19-year-olds , who are the academic professor’s strong suit? ] ‘The reality is then that most under-65s will now end up boosting their immunity not through vaccination , but through catching Covid many times . In general, Prof Finn says each new infection should feel milder with the length of time you are sick reduced [sic] . “Each time you catch it, your immunity gets stronger and broader ,” he adds. ’ ❂ [ Note : This is simply not true, and is staggeringly dangerous. ] ❂ 📖 (24 Sep 2023 ~ Jim Reed, Health Reporter / BBC online) What you need to know about Covid as new variant [BA.2.86] rises ➤ © 2023 BBC .

📖 On Lymphocytopenia

by Merck and Co. • 16 Sept, 2023
❦ ‘The most common causes of acquired lymphocytopenia include: ➲ Protein-energy undernutrition. ➲ HIV infection. ➲ COVID-19 . ➲ Certain other viral infections. Patients with HIV infection routinely have lymphocytopenia, which arises from destruction of CD4+ T cells infected with the HIV virus. Patients with COVID-19 also frequently have lymphocytopenia ( 35% to 83% of patients ) . Lower lymphocyte counts portend a poor prognosis and an increased likelihood of requiring ICU admission and of dying from the disease. The cause of the lymphocytopenia is not completely understood, but COVID-19 can directly infect lymphocytes, and a cytokine-related apoptosis of the cells is likely. ➲ Lymphocytopenia is most often due to AIDS , and recently COVID-19 , or undernutrition, but it also may be inherited or caused by various infections, drugs, or autoimmune disorders. ➲ Patients have recurrent viral , bacterial , fungal , or parasitic infections .’ ❂ 📖 (Accessed 16 Sep 2023 ~ Merck & Co.) Entry for 'Lymphocytopenia' in Merck Manual ➤ © 2023 Merck & Co .

On immune systems, and chewing on the leftovers

by Dr. Noor Bari, Emergency Medicine • 27 Aug, 2023
❦ 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. © 2023 Dr. Noor Bari . ➲

📖 The immunology of long COVID

by Altmann et al / Nature • 11 Jul, 2023
❦ ‘Long COVID is the patient-coined term for the disease entity whereby persistent symptoms ensue in a significant proportion of those who have had COVID-19, whether asymptomatic, mild or severe. The disease burden spans from mild symptoms to profound disability, the scale making this a huge, new healthcare challenge. Long COVID will likely be stratified into several more or less discrete entities with potentially distinct pathogenic pathways. The evolving symptom list is extensive, multi-organ, multisystem and relapsing–remitting, including fatigue, breathlessness, neurocognitive effects and dysautonomia. A range of radiological abnormalities in the olfactory bulb, brain, heart, lung and other sites have been observed in individuals with Long COVID. Some body sites indicate the presence of microclots; these and other blood markers of hypercoagulation implicate a likely role of endothelial activation and clotting abnormalities. Diverse auto-antibody (AAB) specificities have been found, as yet without a clear consensus or correlation with symptom clusters. There is support for a role of persistent SARS-CoV-2 reservoirs and/or an effect of Epstein-Barr virus reactivation, and evidence from immune subset changes for broad immune perturbation. The oncoming burden of Long COVID faced by patients, healthcare providers, governments and economies is so large as to be unfathomable, which is possibly why minimal high-level planning is currently allocated to it.’ ❂ 📖 (11 July 2023 ~ Nature Reviews: Immunology) The immunology of long COVID ➤ © 2023 Altmann et al / Nature.

📖 SARS-CoV-2 and “Textbook” Immunity

by The John Snow Project • 05 May, 2023
❦ Prior to 2020, there were four endemic human coronaviruses – OC43, NL-63, 229E, and HKU1 – which were known to cause 10 to 15 percent of common colds – or the ‘Common Cold Coronaviruses’ (CCCs).  From at least the 1970s, we’ve known that infection with these coronaviruses does not lead to lasting protection from reinfection – this is textbook knowledge. CCCs are not just colds – they can cause severe pneumonias, and exhibit a risk profile very similar to SARS-CoV-2 with age. If reinfection really did strengthen immunity against CCCs, then older people would be the least affected – because they would have been regularly infected with diverse variants of these viruses in their past. But that is not the case – and SARS-CoV-2 is not a CCC. SARS-CoV-2 has a wide array of accessory proteins that silence and disrupt our normal immune responses. As we get older, our immune systems start to lose their effectiveness – and we become more susceptible to disease. This process is called immunosenescence . Repeated exposure to a virus like SARS-CoV-2 is fast-tracking more people into immunosenescence at ever-earlier ages, with potentially serious repercussions for their health and longevity. SARS-CoV-2 is a particularly nasty virus that can also trigger the hyperactivation of our own immune systems to cause severe disease. Infection by SARS-CoV-2 has been shown to lead to an increase in autoantibodies and autoimmune disease. Approximately 25 percent of people who develop an autoimmune disease will experience multiple autoimmune syndrome, and will risk a cascade of autoimmune conditions. SARS-CoV-2, like its 2002 predecessor SARS-CoV-1, is both a respiratory and a systemic virus, with an extremely broad cell-type and tissue-tropism covering nearly the whole body. Its ability to infect and do damage to lungs, hearts, kidneys, cardiovascular systems and brains is particularly well-documented. If each subsequent infection results in additional internal organ and immune-system damage, then at some point the damage accumulated – together with the accelerated immune-system aging and normal aging processes – can reasonably be expected to outweigh the protective benefits of immunity developed from previous infections. SARS-CoV-2 reinfects more frequently than influenza or the common cold, infects a wider range of organs, does more damage and seems capable of persisting in a range of organs. So if SARS-CoV-2 behaves like a textbook virus – but does more damage more quickly and more regularly – at what point does the body reach its tipping point? ❂ There are two versions of this article: a 7-minute read in simplified language ; and the full editorial version complete with references, which is an 18-minute-read and aimed towards the medical and scientific communities . ❦ 7-minute primer ~ ‘SARS-CoV-2 and “Textbook” Immunity’ ➤ ❦ Full 18-minute editorial ~ ‘SARS-CoV-2 and “Textbook” Immunity’ ➤ ❂ 📖 (5 May 2023 ~ The John Snow Project) SARS-CoV-2 and "Textbook" Immunity ➤ © 2023 The John Snow Project.

📖 Fungal infection profile in critically ill COVID-19 patients: a prospective study at a large teaching hospital in a middle-income country

by Negm et al / BMC Infectious Diseases • 23 Apr, 2023
❦ Critically ill COVID-19 patients are highly susceptible to opportunistic fungal infection due to many factors, including virus-induced immune dysregulation , host-related comorbidities, overuse and misuse of antibiotics or corticosteroids, immune modulator drugs, and the emergencies caused by the pandemic. Fungal coinfection is a common complication of critically ill COVID-19 patients admitted to the ICU. Candidiasis , aspergillosis , and mucormycosis are the most common COVID-19-associated fungal infections and have a great impact on mortality rates . ❂ 📖 (18 Apr 2023 ~ BMC Infectious Diseases) Fungal infection profile in critically ill COVID-19 patients: a prospective study at a large teaching hospital in a middle-income country ➤ © 2023 Negm et al / BMC Infectious Diseases.

📖 Status of major hemostatic components in the setting of COVID-19: the effect on endothelium, platelets, coagulation factors, fibrinolytic system, and complement

by Sayyadi et al / Annals of Hematology • 19 Apr, 2023
❦ ‘COVID-19 patients have a hypercoagulability state, and thrombosis is a life-threatening complication of them.’ ✻ Hypercoagulability , also known as thrombophilia , is a condition in which there is an abnormally increased tendency towards blood clotting . ‘From the early days of the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) outbreak to the present, clinical and basic studies have indicated that coronavirus disease 2019 (COVID-19) may be associated with coagulopathy ( CAC ), which is involved in its related morbidity and mortality. Deep vein thrombosis ( DVT ) and pulmonary embolism ( PE ) are common in COVID-19 patients and are remarkably high in the intensive care unit (ICU)–admitted patients. CAC can lead to the formation of circulating microthrombi and macrothrombi which can involve multiple sites, including the lungs , brain , heart , and visceral organs like kidneys and spleen . There is a close relationship between the immune system and coagulation. The components of the hemostatic system play a role in the body’s immunity, and the activation of the immune system strongly influences the hemostatic system. Abnormal activation of the immune system may promote the growth of pathologies associated with thrombosis. COVID-19 is accompanied by an immune-cell hyperactivation and excessive production of proinflammatory cytokines , known as “ cytokine storm ”. CAC is theorized to result from dysregulated interactions between the immune and coagulation systems .’ ❂ 📖 (19 Apr 2023 ~ Annals of Hematology) Status of major hemostatic components in the setting of COVID-19: the effect on endothelium, platelets, coagulation factors, fibrinolytic system, and complement ➤ © 2023 Annals of Hematology .

📖 Long-term risk of herpes zoster [shingles] following COVID-19: A retrospective cohort study of 2,442,686 patients

by Chen et al / Journal of Medical Virology • 18 Apr, 2023
❦ 'The risk of herpes zoster (HZ) ( Shingles ) remained significantly [+60%] higher in patients with COVID-19 compared with those without COVID-19. The higher risk of HZ in the COVID-19 cohort compared with that in the non-COVID-19 cohort remained consistent across subgroup analyses regardless of vaccine status, age, or sex. The risk of HZ within a 12-month follow-up period was significantly higher in patients who had recovered from COVID-19 compared with that in the control group. ❂ 📖 (18 Apr 2023 ~ Journal of Medical Virology) Long-term risk of herpes zoster following COVID-19: A retrospective cohort study of 2 442 686 patients ➤ © 2023 Journal of Medical Virology.

📖 High risk of autoimmune diseases after COVID-19

by Sharma & Jagadeesh / Nature Reviews: Rheumatology • 12 Apr, 2023
❦ The full picture of post-COVID-19 autoimmune diseases and their prevalence is lacking despite numerous case reports and small series. Two studies that use large cohorts now highlight that SARS-CoV-2 infection is linked to a substantially increased risk of developing a diverse spectrum of new-onset autoimmune diseases . The reports by Chang et al and Tesch et al provide a comprehensive overview of diverse new-onset autoimmune conditions after COVID-19. In addition, an earlier preprint of a retrospective matched cohort analysis using data from the Clinical Practice Research Datalink Aurum database of 458,147 SARS-CoV-2-infected and 1,818,929 uninfected adults across England between 31 January 2020 and 30 June 2021 reported that the incidence of type 1 diabetes mellitus , inflammatory bowel disease and psoriasis are significantly associated with SARS-CoV-2 infection. Some of the earliest evidence that SARS-CoV-2 infection leads to dysregulated immune responses came from paediatric patients who presented with multisystem inflammatory syndrome in children (MIS-C) , which, as the name indicates, involves diffuse organ system involvement and a clinical spectrum that overlaps with other hyperinflammatory syndromes , such as Kawasaki disease , toxic-shock syndrome , and macrophage activation syndrome . Since the start of the pandemic, many researchers have also reported isolated cases of adults with various post-COVID-19 autoimmune conditions. ❂ 📖 (12 Apr 2023 ~ Nature Reviews: Rheumatology) High risk of autoimmune diseases after COVID-19 ➤ © 2023 Sharma & Jagadeesh / Nature.

📖 SARS-CoV-2 infection of thymus induces loss of function that correlates with disease severity

by Rosichini et al / Journal of Allergy and Clinical Immunology • 07 Feb, 2023
❦ Lymphopenia , particularly when restricted to the T-cell compartment, has been described as one of the major clinical hallmarks in patients with coronavirus disease 2019 ( COVID-19 ) and proposed as an indicator of disease severity. Although several mechanisms fostering COVID-19-related lymphopenia have been described, including cell apoptosis and tissue homing, the underlying causes of the decline in T-cell count and function are still not completely understood. Patients with COVID-19 had reduced thymic function that was inversely associated with the severity of the disease. Our data demonstrate that the human thymus is a target of SARS-CoV-2 and thymic function is altered following infection . Note: Lymphopenia (also called lymphocytopenia) is a disorder in which your blood doesn't have enough white blood cells called lymphocytes. Lymphocytes play a protective role in your immune system. ❂ 📖 (7 Feb 2023 ~ Journal of Allergy and Clinical Immunology) SARS-CoV-2 infection of thymus induces loss of function that correlates with disease severity ➤ © 2023 Rosichini e t al / Journal of Allergy and Clinical Immunology.

📖 Children's immune systems do not develop 'adaptive memory' to protect against second-time SARS-CoV-2 infection

by Emily Henderson / Medical Life Sciences • 26 Jan, 2023
❦ ‘Children have largely avoided severe COVID-19 symptoms because they have a strong initial ‘innate’ immune reaction that quickly defeats the virus. But unlike those of adults, children’s immune systems don’t remember the virus and don’t adapt, so when they’re next exposed to SARS-CoV-2, their body still treats it as a new threat. “Because children haven’t been exposed to many viruses, their immune system is still ‘naive’. And because they don't develop memory T cells, they are at risk of getting sick when they become reinfected. With each new infectious episode as they get older, there is a risk of their T cells becoming ‘exhausted’ and ineffective, like the T cells in older people. 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,” says Professor Tri Phan.’ ❂ 📖 (26 Jan 2023 ~ Medical Life Sciences) Children's immune systems do not develop 'adaptive' memory to protect against second-time SARS-CoV-2 infection ➤ 📖 (January 2023 ~ Clinical Immunology) Tracking the clonal dynamics of SARS-CoV-2-specific T cells in children and adults with mild/asymptomatic COVID-19 ➤ © 2023 Emily Henderson / Medical Life Sciences.

📖 New insights into deadly fungal invasion in people with compromised immune systems

by Emily Henderson / News Medical Life Sciences • 12 Jan, 2023
❦ Fungi such as Aspergillus are so common in our surroundings that we breathe in hundreds to thousands of spores every day. In healthy people, fungi typically pose no threat, but they can cause deadly infections in those with compromised immune systems. However, it is increasingly recognized that viral infections such as influenza or SARS-CoV-2 can increase the risk of invasive Aspergillus infections even in healthy people. ❂ 📖 (12 Jan 2023 ~ News-Medical.Net) New insights into deadly fungal invasion in people with compromised immune systems ➤ © 2023 Emily Henderson / News Medical Life Sciences.

📖 Immune systems seriously weakened by COVID

by Terry Pender / Waterloo Region Record • 20 Dec, 2022
❦ Evolving research says COVID leaves many people at heightened risk for other infections. SARS-CoV-2 depletes the body’s supply of T-cells, * leaving young and old alike vulnerable to secondary infections. * (T-cells are the ‘front-line soldiers’ of the immune system, and the number of T-cells typically increases when the body is fighting off an infection.) “Individuals who are infected with COVID have many fewer T-cells – that’s a problem for us, because T-cells are a really important part of our immune system that helps defend us against infection.” But at least three studies show ✢ that COVID kills off a significant number of the body’s T-cells – so even when someone recovers from COVID, they are at a heightened risk for other viral, bacterial and fungal infections. “With the loss of these T-cells, we are now more vulnerable to all of these other infections, other viruses, other bacteria.” COVID-19 sparks what is called ‘programmed cell death’ among T-cells. Cells in the human body do this naturally as they age, but COVID-19 causes healthy T-cells to die that would otherwise be available to fight off infections. Many people who have had COVID brush it off, saying it was no worse than a bad case of the flu. What they don’t know is that they are more vulnerable to secondary infections that may cause them to seek help at a hospital emergency ward. ❂ ✢ 📖 (11 Jan 2023 ~ Nature Reviews / Immunology) Innate immune evasion strategies of SARS-CoV-2 ➤ 📖 (13 Jan 2023 ~ Preprint) Structure-based discovery of inhibitors of the SARS-CoV-2 Nsp14 N7-methyltransferase ➤ 📖 20 Apr 2021 ~ Nature / Cell Death & Differentiation) SARS-CoV-2 spike protein dictates syncytium-mediated lymphocyte elimination ➤ ❂ 📖 (20 Dec 2022 ~ Waterloo Region Record) Immune systems seriously weakened by COVID ➤ © 2022 Terry Pender / Waterloo Region Record.

📖 COVID-19 disease and immune dysregulation

by Davitt et al / Best Practice & Research Clinical Haematology • 06 Dec, 2022
❦ While COVID-19 was originally characterized as hyperinflammatory in its pathophysiology, emerging evidence demonstrates the possibility of a strongly immunosuppressive phenotype in more critical disease states. While immune activation from neutrophils and complement may contribute to inflammatory damage in the lungs, decreased antiviral responses, dysregulated macrophages and dendritic cells, and severe lymphopenia contribute to a suppressed state in which viral replication and secondary infections are prone. ❂ 📖 (6 Dec 2022 ~ Best Practice & Research Clinical Haematology) COVID-19 disease and immune dysregulation ➤ © 2022 Davitt et al / Best Practice & Research Clinical Haematology.

On post-COVID infections, immunodeficient patients and multi-drug-resistant diseases

by Dr. Noor Bari, Emergency Medicine • 10 Nov, 2022
❦ This morning someone said to me: — “I just can’t shake this... first a chest infection, and now a urine infection...” Someone else I know (very close) has had three eye infections post-COVID. Another has had a deterioration in their fertility, as compared to their baseline pre- and post-COVID. Measured. It’s almost as if the stuff in the science papers is real. None of them have twigged that COVID might have toasted them yet either. They are all heading into this next wave with no idea how dangerous it might be to abuse their already struggling immune system like this. You know what’s coming next... Multi-drug-resistant bacteria. Many are already here, but this is going to get really out of control. Trying to treat infections in immunodeficient patients is a great way to make loads of drug-resistant bacteria and viruses. ❂ 📖 (24 May 2023 ~ Current Microbiology) Interaction Between SARS-CoV-2 and Pathogenic Bacteria ➤ 📖 (18 Apr 2023 ~ BMC Infectious Diseases) Fungal infection profile in critically ill COVID-19 patients: a prospective study at a large teaching hospital in a middle-income country ➤ 📖 (29 Mar 2023 ~ Journal of Fungi) Fungal-Bacterial Co-Infections and Super-Infections among Hospitalized COVID-19 Patients: A Systematic Review ➤ 📖 (30 Sep 2021 ~ Insider) Drug-resistant infections in the US have risen sharply during the pandemic, and experts warn it's getting worse as COVID patients overwhelm hospital resources ➤ © 2022 Dr. Noor Bari, Emergency Medicine ➲

On immunological dysfunction and post-COVID infections

by Dr. Noor Bari, Emergency Medicine • 30 Oct, 2022
❦ COVID-19 is fighting back by generally depressing the whole adaptive immune system. We are showing narrow resilience to COVID reinfections due to adapting – but we are becoming more vulnerable in general to infections of all kinds. ❦ Worst case scenario: a single infection causes on-going and progressive immunodeficiency . ❦ Best case scenario: a single infection causes temporary immunosuppression , and we suppress COVID transmission enough to allow recovery. ❦ Most likely scenario, medium-term: immunosuppression that becomes continuous and possibly progressive due to reinfections. Reduced immune function after a viral infection is not unusual. Many viruses do this. The concerning issue is the length and breadth of the immune system dysfunction, coupled with emerging evidence of other pathogens taking advantage. ❂ ❦ Immunosuppression ~ Suppression of the immune system and its ability to fight infection. ❦ Immunodeficiency ~ A state in which the immune system's ability to fight infectious diseases and cancer is compromised, or entirely absent. ❂ 📖 (13 Jan 2022 ~ Nature: Immunology) Immunological dysfunction persists for 8 months following initial mild-to-moderate SARS-CoV-2 infection ➤ © 2022 Dr. Noor Bari, Emergency Medicine ➲

📖 When COVID-19 or flu viruses kill, they often have an accomplice – bacterial infections

by Hayley Muendlein / The Conversation • 17 Aug, 2022
❦ The 1918 influenza pandemic resulted in the loss of over 3% of the world’s population – at least 50 million people. But it wasn’t the flu virus that caused the majority of these deaths. An analysis of lung samples collected during that flu pandemic indicated that most of the deaths were likely due to bacterial pneumonia , which ran rampant in the absence of antibiotics. Even in more recent history, like the 1957 H2N2 and 2009 H1N1 flu pandemics , nearly 18% of patients with viral pneumonia had additional bacterial infections that increased their risk of death. And the COVID-19 pandemic is no different. ❂  📖 (17 Aug 2022 ~ The Conversation) When COVID-19 or flu viruses kill, they often have an accomplice – bacterial infections ➤ © 2022 Hayley Muendlein / The Conversation.

On bat-like immune systems, and ‘living with the virus’

by Dr. Noor Bari, Emergency Medicine • 21 Jul, 2022
❦ So, we want to ‘live with the virus’. Is there any evidence of this occurring successfully anywhere? Yes! In bats... and it has taken 64 million years of evolution ✢ to get there. 📖 (20 Jan 2021 ~ Nature) Lessons from the host defences of bats, a unique viral reservoir ➤ To ‘live with the virus’, bats have better host defences – they don’t overdo inflammation, and they can get rid of toxic compounds and deal with reactive oxygen species much better than humans. They literally live with the virus . For humans to ‘live with the virus’, we would need to have similar mechanisms to permit SARS-CoV-2 to be part of our biome – without causing all of the autoimmune disease and other damage. We would have to have fundamentally different biochemistry and immune systems. We can mimic this using therapeutics to some extent, and this may help us treat Long COVID. However, I don’t think that we will naturally become resilient to SARS-CoV-2 for a very long time. What I’m trying to say is that mass-infecting this generation of children is unlikely to result in them developing a bat-like immune system within their lifetimes. It’s ridiculous that the attempt was ever made. I genuinely think that putting ventilation upgrades into every building and wearing good-quality masks will be easier than building a genetically modified SARS-resistant human. I keep trying to give you the easy way out! The coronavirus is moving into our bodies and is attempting to stay there, just like it does in bats. The problem is that our bodies try to fight it. We fight it well enough to reduce detectable virus-shedding on our breath, but there is evidence (persistent spike RNA) that the virus is hiding somewhere else in our body anyway. So our bodies keep fighting it. The collateral damage is the problem. What are our choices? 1. Figure out how to change human physiology so that we don’t burn ourselves out fighting an elusive and persistent enemy. 2. Or figure out how we can stop transmission. The second is easier, and economically sound. The ability to completely clear coronavirus is also a potential goal – but again, therapeutics will be needed because we have places where, if the immune system is left to do it, it causes damage – and coronavirus has many tricks to help it hide from detection. Needless to say, coronavirus can evolve a lot faster than we can, so we need to use our brain cells in a different way to fight COVID-19. Instead of using microglia, we need to think ...

📖 Coronavirus Deranges the Immune System in Complex and Deadly Ways

by Liz Szabo / KFF Health News • 04 Mar, 2021
❦ While all viruses find ways to evade the body’s defenses, a growing field of research suggests that the coronavirus unhinges the immune system more profoundly than previously realized. Some Covid survivors have developed serious autoimmune diseases, which occur when an overactive immune system attacks the patient, rather than the virus. Doctors in Italy first noticed a pattern in March 2020, when several Covid patients developed Guillain-Barré syndrome, in which the immune systems attacks nerves throughout the body, causing muscle weakness or paralysis. As the pandemic has surged around the world, doctors have diagnosed patients with rare, immune-related bleeding disorders. Other patients have developed the opposite problem, suffering blood clots that can lead to stroke. All these conditions can be triggered by autoantibodies – rogue antibodies that target the patient’s own proteins and cells. ❂ 📖 (4 Mar 2021 ~ KFF Health News) Coronavirus Deranges the Immune System in Complex and Deadly Ways ➤ © 2021 Liz Szabo / KFF Health News.

❦ on immunity: scientific papers & media articles

✒ 2023

📖 (Accessed 20 Sep 2023 ~ University of Oxford) Autoimmune disorders found to affect around one in ten people ➤


❂


📖 (13 Sep 2023 ~ 1 News/NZ) Covid may have permanently damaged people's immunity ➤


❂


📖 (18 Aug 2023 ~ Cell) Epigenetic memory of coronavirus infection in innate immune cells and their progenitors ➤


❂


📖 (16 Aug 2023 ~ The Lancet / eClinicalMedicine) Risk of autoimmune diseases following COVID-19 and the potential protective effect from vaccination: a population-based cohort study ➤


❂


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


❂


📖 (4 Aug 2023 ~ Pre-print) Long COVID manifests with T cell dysregulation, inflammation, and an uncoordinated adaptive immune response to SARS-CoV-2 ➤


❂


📖 (19 Jun 2023 ~ Clinical Rheumatology) Incident autoimmune diseases in association with SARS-CoV-2 infection: a matched cohort study ➤


❂


📖 (3 Jun 2023 ~ The Lancet) Incidence, prevalence, and co-occurrence of autoimmune disorders over time and by age, sex, and socioeconomic status: a population-based cohort study of 22 million individuals in the UK ➤


❂


📖 (3 May 2023 ~ Infectious Diseases) Evaluation of Waning of SARS-CoV-2 Vaccine-Induced Immunity – A Systematic Review and Meta-analysis ➤


❂


📖 (25 Apr 2023 ~ International Journal of Molecular Sciences) Deciphering the Relationship between SARS-CoV-2 and Cancer ➤

 

➲ 'Some viruses are known to be associated with the onset of specific cancers.


These micro-organisms, oncogenic viruses or oncoviruses, can convert normal cells into cancer cells by modulating the central metabolic pathways or hampering genomic integrity mechanisms, consequently inhibiting the apoptotic machinery and/or enhancing cell proliferation.


Seven oncogenic viruses are known to promote tumorigenesis [the formation of a cancer] in humans: human papillomavirus (HPV) [associated with genital warts], hepatitis B and C viruses (HBV, HCV), Epstein-Barr virus (EBV) [human herpesvirus 4], human T-cell leukemia virus 1 (HTLV-1), Kaposi sarcoma-associated herpesvirus (KSHV), and Merkel cell polyomavirus (MCPyV).


Recent research indicates that SARS-CoV-2 infection and COVID-19 progression may predispose recovered patients to cancer onset and accelerate cancer development.'


❂


📖 (18 Apr 2023 ~ Journal of Medical Virology) Long-term risk of herpes zoster following COVID-19: A retrospective cohort study of 2 442 686 patients ➤

 

➲ 'The risk of herpes zoster (HZ) (Shingles) remained significantly [+60%] higher in patients with COVID-19 compared with those without COVID-19.


The higher risk of HZ in the COVID-19 cohort compared with that in the non-COVID-19 cohort remained consistent across subgroup analyses regardless of vaccine status, age, or sex.


The risk of HZ within a 12-month follow-up period was significantly higher in patients who had recovered from COVID-19 compared with that in the control group.'


❂


📖 (18 Apr 2023 ~ BMC Infectious Diseases) Fungal infection profile in critically ill COVID-19 patients: a prospective study at a large teaching hospital in a middle-income country ➤

 

➲ 'Critically ill COVID-19 patients are highly susceptible to opportunistic fungal infection due to many factors, including virus-induced immune dysregulation, host-related comorbidities, overuse and misuse of antibiotics or corticosteroids, immune modulator drugs, and the emergencies caused by the pandemic.


Fungal coinfection is a common complication of critically ill COVID-19 patients admitted to the ICU. Candidiasis, aspergillosis, and mucormycosis are the most common COVID-19-associated fungal infections and have a great impact on mortality rates.'


❂


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

 

➲ 'Reinfection with SARS-CoV-2 does occur, suggesting that natural immunity is not long-lasting in COVID-19 patients. Female patients seem more likely to experience reinfection than male patients.


Thus far, no clear evidence for a difference in severity between the first infection and reinfection has been observed.'


❂


📖 (12 Apr 2023 ~ Nature Reviews: Rheumatology) High risk of autoimmune diseases after COVID-19 ➤

 

➲ 'Two studies that use large cohorts now highlight that SARS-CoV-2 infection is linked to a substantially increased risk of developing a diverse spectrum of new-onset autoimmune diseases.


The reports by Chang et al and Tesch et al provide a comprehensive overview of diverse new-onset autoimmune conditions after COVID-19.


In addition, an earlier preprint of a retrospective matched cohort analysis using data from the Clinical Practice Research Datalink Aurum database of 458,147 SARS-CoV-2-infected and 1,818,929 uninfected adults across England between 31 January 2020 and 30 June 2021 reported that the incidence of type 1 diabetes mellitus, inflammatory bowel disease and psoriasis are significantly associated with SARS-CoV-2 infection.'


❂


📖 (21 Mar 2023 ~ Infection Control Today) COVID-19: Study Suggests Long-term Damage to Immune System ➤


❂


📖 (March 2023 ~ Asia Pacific Allergy) Immunological dysfunction and mast cell activation syndrome in long COVID ➤


❂


📖 (16 Feb 2023 ~ BMC Biology) High SARS-CoV-2 tropism and activation of immune cells in the testes of non-vaccinated deceased COVID-19 patients ➤


❂


📖 (7 Feb 2023 ~ Journal of Allergy and Clinical Immunology) SARS-CoV-2 infection of thymus induces loss of function that correlates with disease severity ➤

 

➲ 'Lymphopenia, particularly when restricted to the T-cell compartment, has been described as one of the major clinical hallmarks in patients with coronavirus disease 2019 (COVID-19) and proposed as an indicator of disease severity.


Although several mechanisms fostering COVID-19-related lymphopenia have been described, including cell apoptosis and tissue homing, the underlying causes of the decline in T-cell count and function are still not completely understood.


Patients with COVID-19 had reduced thymic function that was inversely associated with the severity of the disease.


Our data demonstrate that the human thymus is a target of SARS-CoV-2 and thymic function is altered following infection.'


Note: Lymphopenia (also called lymphocytopenia) is a disorder in which your blood doesn't have enough white blood cells called lymphocytes. Lymphocytes play a protective role in your immune system.


❂


📖 (18 Jan 2023 ~ Nature) How your first brush with COVID warps your immunity ➤


❂


📖 (13 Jan 2023 ~ Preprint) Structure-based discovery of inhibitors of the SARS-CoV-2 Nsp14 N7-methyltransferase ➤


❂


📖 (12 Jan 2023 ~ News-Medical.Net) New insights into deadly fungal invasion in people with compromised immune systems ➤

 

➲ 'Fungi such as Aspergillus are so common in our surroundings that we breathe in hundreds to thousands of spores every day.


In healthy people, fungi typically pose no threat, but they can cause deadly infections in those with compromised immune systems.


However, it is increasingly recognized that viral infections such as influenza or SARS-CoV-2 can increase the risk of invasive Aspergillus infections even in healthy people.'


❂


📖 (11 Jan 2023 ~ Nature Reviews: Immunology) Innate immune evasion strategies of SARS-CoV-2 ➤


❂


📖 (January 2023 ~ Clinical Immunology) Tracking the clonal dynamics of SARS-CoV-2-specific T cells in children and adults with mild/asymptomatic COVID-19 ➤


❂

✒ 2022

📖 (26 Dec 2022 ~ Nature) Transcriptional reprogramming from innate immune functions to a pro-thrombotic signature by monocytes in COVID-19 ➤


❂


📖 (6 Dec 2022 ~ Best Practice & Research Clinical Haematology) COVID-19 disease and immune dysregulation ➤

 

➲ 'While COVID-19 was originally characterized as hyperinflammatory in its pathophysiology, emerging evidence demonstrates the possibility of a strongly immunosuppressive phenotype in more critical disease states.


While immune activation from neutrophils and complement may contribute to inflammatory damage in the lungs, decreased antiviral responses, dysregulated macrophages and dendritic cells, and severe lymphopenia contribute to a suppressed state in which viral replication and secondary infections are prone.'


❂


Note: ❊ = Scientific paper illustrating clear immune dysregulation.


❊ 📖 (2 Dec 2022 ~ Frontiers in Immunology) Single-cell multiomics revealed the dynamics of antigen presentation, immune response and T cell activation in the COVID-19 positive and recovered individuals ➤


❂


❊ 📖 Preprint: (20 Nov 2022 ~ medRxiv) Direct Cryo-ET observation of platelet deformation induced by SARS-CoV-2 Spike protein ➤


❂


❊ 📖 Preprint: (20 Nov 2022 ~ medRxiv) Elevated circulating monocytes and monocyte activation in pulmonary post-acute sequelae of SARS-CoV-2 infection ➤


❂


📖 (22 Oct 2022 ~ Cleveland.com) In Cleveland and beyond researchers begin to unravel the mystery of long COVID-19 ➤


❂


📖 (7 Oct 2022 ~ Counter Disinformation Project) "Immunity Debt"? Established 2021 ➤


❂


📖 (22 Sep 2022 ~ European Respiratory Journal) Circulating anti-nuclear autoantibodies in COVID-19 survivors predict long COVID symptoms ➤


❂


📖 (12 Sep 2022 ~ Nature: Communications) Previous immunity shapes immune responses to SARS-CoV-2 booster vaccination and Omicron breakthrough infection risk ➤


❂


📖 (17 Aug 2022 ~ The Conversation) When COVID-19 or flu viruses kill, they often have an accomplice – bacterial infections ➤

 

➲ 'The 1918 influenza pandemic resulted in the loss of over 3% of the world's population – at least 50 million people.


But it wasn't the flu virus that caused the majority of these deaths.


An analysis of lung samples collected during that flu pandemic indicated that most of the deaths were likely due to bacterial pneumonia, which ran rampant in the absence of antibiotics.


Even in more recent history, like the 1957 H2N2 and 2009 H1N1 flu pandemics, nearly 18% of patients with viral pneumonia had additional bacterial infections that increased their risk of death.


And the COVID-19 pandemic is no different.'


❂


📖 (PDF) (4 Aug 2022 ~ European Respiratory Journal) Circulating anti-nuclear autoantibodies in COVID-19 survivors predict long COVID symptoms ➤


❂


📖 (14 May 2022 ~ Allergy) T-cell recovery and evidence of persistent immune activation 12 months after severe COVID-19 ➤


❂


📖 (1 May 2022 ~ Gastroenterology) Postacute COVID-19 is Characterized by Gut Viral Antigen Persistence in Inflammatory Bowel Diseases ➤


❂


📖 (22 Apr 2022 ~ Clinical Infectious Diseases) Reduced Cell Surface Levels of C-C Chemokine Receptor 5 and Immunosuppression in Long Coronavirus Disease 2019 Syndrome ➤


❂


📖 (8 Apr 2022 ~ Pre-print) SARS-CoV-2 and its variants, but not Omicron, induces thymic atrophy and impaired T cell development ➤


❂


📖 (23 Mar 2022 ~ Pathogens) Superantigens and SARS-CoV-2 ➤


❂


❊ 📖 (11 Mar 2022 ~ Nature Signal Transduction and Targeted Therapy) ACE2-independent infection of T lymphocytes by SARS-CoV-2 ➤


❂


📖 (10 Mar 2022 ~ Science) The immunology and immunopathology of COVID-19 ➤


❂


📖 (3 Mar 2022 ~ Frontiers) Understanding the Effects of Age and T-Cell Differentiation on COVID-19 Severity: Implicating a Fas/FasL-mediated Feed-Forward Controller of T-Cell Differentiation ➤


❂


❊ 📖 (21 Feb 2022 ~ Frontiers in Immunology) Depletion and Dysfunction of Dendritic Cells: Understanding SARS-CoV-2 Infection ➤


❂


❊ 📖 (22 Jan 2022 ~ Nature Immunology) Immunological dysfunction persists for 8 months following initial mild-to-moderate SARS-CoV-2 infection ➤


❂


❊ 📖 (14 Jan 2022 ~ BMC Medicine) Long-term perturbation of the peripheral immune system months after SARS-CoV-2 infection ➤

 

❂


📖 (13 Jan 2022 ~ Nature) Immunological dysfunction persists for 8 months following initial mild-to-moderate SARS-CoV-2 infection ➤


❂

✒ 2021

📖 (16 Nov 2021 ~ The Journal of Clinical Investigation) PD-1 blockade counteracts post-COVID-19 immune abnormalities and stimulates the anti-SARS-CoV-2 immune response ➤


❂


📖 (1 Oct 2021 ~ Pathogens) Uncertainty around the Long-Term Implications of COVID-19 ➤


❂


❊ 📖 (22 Sep 2021 ~ Nature / Signal Transduction and Targeted Therapy) SARS-CoV-2 infection causes immunodeficiency in recovered patients by downregulating CD19 expression in B cells via enhancing B-cell metabolism ➤


❂


❊ 📖 (21 July 2021 ~ Nature / Cellular & Molecular Immunology) Dendritic cell deficiencies persist seven months after SARS-CoV-2 infection ➤


❂


📖 (25 May 2021 ~ The Journal of Clinical Investigation) Multisystem inflammatory syndrome in children is driven by zonulin-dependent loss of gut mucosal barrier ➤


❂


📖 (7 May 2021 ~ Frontiers in Immunology) Longitudinal Analysis of COVID-19 Patients Shows Age-Associated T Cell Changes Independent of Ongoing Ill-Health ➤


❂


📖 (20 Apr 2021 ~ Autoimmunity Reviews) Granulomatous manifestations associated with COVID19 infection: Is there a link between these two diseases? ➤


➲ 'Covid infections are putting people at higher risk of diabetes, strokes, heart disease and other long-term illnesses – but experts warn it may be decades before the full impact is known.'


❂


📖 (21 Mar 2021 ~ Journal of Cosmetic Dermatology) Oral candidiasis of COVID‐19 patients: Case report and review of evidence ➤


❂


📖 (11 Mar 2021 ~ The Journal of Clinical Investigation) HLA class I-associated expansion of TRBV11-2 T cells in multisystem inflammatory syndrome in children ➤


❂


📖 (4 Mar 2021 ~ KFF Health News) Coronavirus Deranges the Immune System in Complex and Deadly Ways ➤

 

➲ 'While all viruses find ways to evade the body's defenses, a growing field of research suggests that the coronavirus unhinges the immune system more profoundly than previously realized.


Some covid survivors have developed serious autoimmune diseases, which occur when an overactive immune system attacks the patient, rather than the virus.


Doctors in Italy first noticed a pattern in March 2020, when several covid patients developed Guillain-Barré syndrome, in which the immune systems attacks nerves throughout the body, causing muscle weakness or paralysis.


As the pandemic has surged around the world, doctors have diagnosed patients with rare, immune-related bleeding disorders. Other patients have developed the opposite problem, suffering blood clots that can lead to stroke.


All these conditions can be triggered by autoantibodies – rogue antibodies that target the patient's own proteins and cells.'


❂

✒ 2020

📖 (21 Dec 2020 ~ Frontiers in Immunology) Akt-Fas to Quell Aberrant T Cell Differentiation and Apoptosis in Covid-19 ➤


❂


📖 (18 Nov 2020 ~ Science / Translational Medicine) Prothrombotic autoantibodies in serum from patients hospitalized with COVID-19 ➤


❂


📖 (17 Nov 2020 ~ Nature) Immune suppression in the early stage of COVID-19 disease ➤


❂


❊ 📖 (29 Oct 2020 ~ The Journal of Clinical Investigation) Sustained cellular immune dysregulation in individuals recovering from SARS-CoV-2 infection ➤


❂


❊ 📖 (28 Sept 2020 ~ Nature / Scientific Reports) Immune dysfunction following COVID-19, especially in severe patients ➤


❂


📖 (24 Sep 2020 ~ Science) Autoantibodies against type I IFNs in patients with life-threatening COVID-19 ➤


❂


📖 (17 Sep 2020 ~ Cell) Severe COVID-19 Is Marked by a Dysregulated Myeloid Cell Compartment ➤


❂


📖 (16 Sep 2020 ~ The Scientist) The Immune Hallmarks of Severe COVID-19 ➤

 

➲ 'Researchers are trying to make sense of immune systems gone haywire and develop biomarkers to predict who will become the sickest from a coronavirus infection.'


“Perhaps severe COVID-19 isn't a purely inflammatory disease, but rather a dangerous loop of ineffective human immune responses and continuous tissue inflammation.”


❂


📖 (16 July 2020 ~ Pre-print) AIDS and COVID-19 are two diseases separated by a common lymphocytopenia ➤


❂


📖 (29 June 2020 ~ PNAS) Superantigenic character of an insert unique to SARS-CoV-2 spike supported by skewed TCR repertoire in patients with hyperinflammation ➤


❂


📖 20 Apr 2021 ~ Nature: Cell Death & Differentiation) SARS-CoV-2 spike protein dictates syncytium-mediated lymphocyte elimination ➤


❂


❊ 📖 (1 May 2020 ~ Frontiers in Immunology) Reduction and Functional Exhaustion of T Cells in Patients With Coronavirus Disease 2019 (COVID-19) ➤


❂


Acknowledgement


My sincere thanks to Andrew Ewing of The World Health Network for helping to compile this list.


❂

Share by: