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

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

‘ These findings have important implications for understanding the potential impact of COVID-19 on long-term immune function and susceptibility to pathogens . ’

CBC Radio-Canada interview with long COVID [PASC] researcher David Putrino from the Icahn School of Medicine at Mount Sinai in New York.

‘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.’

‘ 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 .’

“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.”

❦ 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 ➲

❦ ‘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 .

❦ ‘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 .

❦ “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.”

❦ ‘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.

❦ 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.

❦ 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.

❦ ‘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 .

❦ 'The risk of herpes zoster (HZ) [ shingles ] remained significantly higher [ +60% ] 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.

❦ 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.

‘We are entering a phase of long COVID and chronic disability.’ ❂ ❦ ‘As the numbers of hospitalizations and deaths are dropping, many individuals declare the pandemic all but over, comforted by the belief that infections are mild and less dangerous than the seasonal flu. However, the scientific literature these last few weeks has been filled with deeply concerning reports. We are entering a phase of long COVID and chronic disability. The number of COVID-19 cases in the United States is unknown since our case reporting system has become unreliable and substantially undercounts cases. In England, as of the week ending March 7, 2023, 1 in 40 people is positive for COVID-19 , and reinfections are frequently occurring. It is estimated that as of November 9, 2022, 94% of the U.S. population has been infected by SARS-CoV-2 , and 65% of the United States population has been infected multiple times . The odds of self-reported long COVID were 28% less after the second infection. Unfortunately, the damage of long COVID from a second infection adds to the first . One of the most concerning long-term effects of COVID-19 is immune dysfunction or hypofunction . Confirmatory research was reported this week, and summarized in a National Institute of Health news release which stated: ‘… findings suggest that SARS-CoV-2 infection damages the CD8⁺ T cell response , an effect akin to that observed in earlier studies showing long-term damage to the immune system after infection with viruses such as hepatitis C or HIV .’ The authors conclude that this dysfunction causes lasting damage and may ‘contribute to long COVID, perhaps rendering patients unable to respond robustly to subsequent infections by SARS-CoV-2 variants or other pathogens .’ * * 📖 (20 Mar 2023 ~ National Institutes for Health) SARS-CoV-2 infection weakens immune-cell response to vaccination ➤ These findings mirror those reported by Files et al who state: ‘Overall, expression of these activation and exhaustion markers indicated more severe immune dysregulation of CD8 ⁺ T cells in the hospitalized group.’ And they found that ‘ CD8⁺ T cell expression of exhaustion markers increased in non-hospitalized individuals over time ’. * * 📖 (4 Jan 2021 ~ Journal of Clinical Investigation) Sustained cellular immune dysregulation in individuals recovering from SARS-CoV-2 infection ➤ The authors’ finding of damage to the immune system “akin” to HIV is very concerning, as is the amplification of this result in the NIH news release. Infection Control Today previously reported that the probable cause of the surges in infections we are seeing is an immune dysfunction caused by COVID-19 . With minimal public health interventions, Sweden also experienced surges in respiratory syncytial virus (RSV) cases. Most recently, Sweden has undergone a significant surge in seasonal flu, with reports from the Public Health Agency of Sweden of unusually severe cases. These [Swedish influenza] cases have occurred in ‘... people under the age of 18 without underlying disease or condition, and have been very seriously ill with complications such as myocarditis or encephalitis.’ Other diseases are also rising , exemplified by reports of record-high severe Streptococcal infections and Candida auris . These spikes in infections caused by multiple pathogens are associated with the SARS-CoV-2 pandemic and the mounting evidence of post-COVID-19 immune dysfunction. Vaccinations can not only reduce the incidence of severe disease, but can also help to prevent long COVID, reducing the incidence by 30% to 40%. However, we have expressed concern regarding the bivalent booster’s effectiveness, and reported a rapid waning of booster-induced immunity in the elderly. [See Footnote.] Recently, researchers from the United States found that the relative bivalent booster effectiveness at 5 to 7 months in preventing hospitalizations relative to monovalent vaccine dosages (2, 3, or 4) was 42% and 59% compared to no vaccination. Using the third vaccine dose as a baseline, the UK Health Security Agency found that an additional (fourth) vaccine dosage had effectiveness against hospitalizations at 10 weeks of only 50% .’ Source: 📖 (21 Mar 2023 ~ Infection Control Today) COVID-19: Study Suggests Long-term Damage to Immune System ➤ ❂ Footnote: On waning vaccine effectiveness * ‘Vaccine effectiveness is an important point. Although much of the younger population received a get-out-of-hospital free card for the latest variant, senior citizens were in its crosshairs. During the last 6 months (since May of 2022), those over the age of 75 had a higher rate of hospitalizations than in the Delta surge; those between the ages of 65 and 75 had approximately the same. Both age groups continue to be at high risk for death and disability. However, data showed that for those 65 years of age and older, the monovalent vaccine’s (2 or more doses) effectiveness for preventing hospitalizations fell to 28% in less than a year. Results were worse for those individuals under 65 years – only 19%.’ * 📖 (24 Feb 2023 ~ Infection Control Today) How Soon Is Another Booster Needed? Durability of Vaccine-Induced Immunity ➤ ❂ © 2023 Infection Control Today . ➲

❦ “I’m vaguely following the chatter on the comparisons of COVID with HIV. I’ve never been a fan of this, because there are so many unanswered questions. One thing I am sure of. Research shows the immune system does get damaged. It does. Which bits? How much? Recovery? What opportunistic infections? Impact on global disease patterns? Impact on animal disease patterns (ecology and food-chain threats)? All questions that will be answered over time. No-one should be surprised by this. It should not be even vaguely controversial. Plenty of viruses damage the immune system. We will find out exactly the extent of the nature of COVID on this aspect of health. Another thing I can say with some certainty. Your chances of recovery from a depressed post-viral immune system will not be improved by further infections. I can see a lot of people directly comparing COVID with HIV. Rest assured. I am concerned. I just don’t find that particular comparison helpful. As many have already pointed out, there are significant differences too. You don’t walk into the supermarket and catch a new strain of HIV starting a whole new acute infection every 6-8 months, for example. But there are also signs that some immune cells are recovering many months after infection too – then again, there are probably reservoirs in the body that could potentially continue to mutate, and then cause other pathology down the line – as some animal coronaviruses do. I think COVID is quite an interesting and horrible disease.  I expect we will see what repeated infections really do as time goes on. Excess deaths are already through the roof. One last attempt to clarify. Trying to make COVID into either a cold, or HIV, and ending up with “half-way between” – when in reality COVID is doing 100% COVID, which is turning out to be really, really bad in its own right… and it’s airborne… and we are catching it all the time. That’s the part I find frustrating with this comparison. SARS is a dangerous, dangerous disease. It always has been. Both of them [SARS (-CoV-1) and SARS-CoV-2] . Yes, there are threads of similarities, and we can use our wealth of knowledge to extrapolate possible outcomes, and test treatments… But SARS is not half-way to anything. It is, in itself, a giant problem.”

❦ 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 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.

❦ 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.

❦ 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.

❦ 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.

❦ “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.” ❂ 📖 (17 May 2024 ~ CIDRAP/University of Minnesota) Global Meta-analysis estimates 43% rate of multidrug resistance in COVID patients➤ 📖 (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 ➤

❦ “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.

❦ “Not catching a common virus for a year or two, or five, does not make you respond to it like an immunosuppressed person the next time you catch it. Avoiding pathogens doesn’t damage your immune system. On the other hand, there are many pathogens out there that are capable of damaging your immune system. Pathogens are foes, not friends.”

❦ 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.

❦ “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. 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 .