An Analysis of the COVID Pandemic

Update, Questions, Summary, References, and Tentative Conclusion

“I have tried to let Truth be my prejudice”

        W. Eugene Smith, photojournalist (1918-1978)*

 

 

 

 

INTRODUCTION:

The purpose of this article is to provide scientific information that will facilitate respectful, healthy dialogue about the COVID pandemic—a profoundly serious problem that threatens all of Humanity and must be accurately and compassionately understood.

From the beginning of the pandemic a spectrum of views on COVID has been apparent. At one end of the spectrum has been the view that COVID has not represented an unusual health threat and the SARS-CoV-2 virus does not even exist. At the other end of the spectrum has been the view that SARS-CoV-2 is so threatening that it absolutely necessitates acceptance of the risks associated with mass vaccination with suboptimal and inadequately studied vaccines, as well as the risks associated with prolonged lockdown measures, until 100% of the world’s population (including children) has been fully vaccinated (i.e., “zero tolerance,” complete eradication of the virus).

Many people have a view that falls somewhere between these two ends of the spectrum. Many may have a view that is not fully formed, because their own questions have not been adequately answered and they remain perplexed, worried, fearful, and uncertain of what to believe and what to do. The vast majority of people simply want to know the truth and want to do the right thing.

Twenty key questions about the COVID pandemic are discussed in this article. Since there have been major differences of opinion regarding many of these questions, I have presented the opposing points of view and suggested that an “Independent International COVID Commission” be formed, consisting of independent international panels of fairly selected, eminent scientists who would be asked to respectfully, thoroughly, objectively, transparently, and publicly address these questions and try to resolve the disagreements. Such is the tradition of science, medicine, democracy, and civil society. The public deserves and desperately needs such careful examination and healthy dialogue, and successful resolution of the COVID pandemic requires such.

The order in which the 20 questions are discussed is based on how a pandemic would usually be analyzed by public health physicians when they use an objective, strictly scientific problem-solving approach—starting with a fundamental first question “how threatening is the virus?” and proceeding to the next logical question. The reader is encouraged, however, to read through the 20 questions in whatever order is most helpful and urgent to them. Many may find it most helpful to start with question 3, then proceed to questions 5-16, then 1, 2, 4, and 17-20 in roughly that order. Please choose whatever order is most helpful for you.

Further discussion of each question (including further references) may be found on a website, entitled Notes from the Social Clinic, where 21 articles on COVID are posted in the second section of the website. (The first section of the website is devoted to discussion of Social Beauty.) The website may be accessed by googling: notesfromthesocialclinic.org

For a quick read of this article, consider going to its end, where you will find a Summary of its tentative conclusions. Those conclusions are drawn “out of an abundance of caution,” until more is known. They may need eventual modification, depending on ongoing research and the results of the thorough examination and healthy dialogue conducted by the aforementioned proposed international panels.

 

1. How deadly was the original SARS-CoV-2 virus?

At the beginning of the COVID pandemic, it was feared that the SARS-CoV-2 virus might represent the most threatening respiratory virus since the deadly 1918 Spanish influenza virus, which was an H1N1 influenza virus of avian origin. [1] The initial concern, advanced by Fauci, et al, was that SARS-CoV-2 might be at least 10 times more deadly than seasonal influenza viruses [2]—though in that same article the authors acknowledged that “the overall clinical consequences of COVID-19 may ultimately be more akin to those of a severe seasonal influenza or a pandemic influenza (similar to those in 1957 and 1968) rather than a disease similar to SARS or MERS, which have had case fatality rates of 9 to 10% and 36%, respectively.”[2]

Out of an abundance of caution, it initially seemed appropriate to implement global lockdown measures, at least briefly, until more was known.

The Infection Fatality Rate (IFR) of SARS-CoV-2: Within several weeks after onset of the epidemic, highly respected epidemiologists (including, most notably, John Ioannides, at Stanford University) determined that the Infection Fatality Rate (IFR) of SARS-CoV-2 was considerably less than initially feared. [3-8] The median IFR across 51 global locations was 0.23% for the population as a whole, and the IFR for people less than 70 years old was 0.05%. [4] According to more recent studies conducted by Ioannides, the IFR of SARS-CoV-2 is particularly low in the younger age groups: specifically, the IFR was 0.0027%, 0.014%, 0.031%, 0.082%, 0.27%, and 0.59% in people aged 0-19, 20-29, 30-39, 40-49, 50-59, and 60-69, respectively. [7] Stating these data in a different way, the odds of dying from SARS-CoV-2 infection are 1 in 37,037 for children and adolescents (those under 20 years of age); 1 in 7,143 for those between 20-29; 1 in 3,226 for those between 30-39; 1 in 1,219 for those between 40-49; 1 in 370 for those between 50-59; and 1 in 169 for those between 60-69. Those odds (the IFR) would be expected to be lower (perhaps much lower) than just stated, if a person has no co-morbidities and/or receives prompt, appropriate treatment (see Question 3).

As is the case with influenza infection, SARS-CoV-2 infection is, of course, much more deadly in people over 69 years of age, particularly in elderly nursing home residents. Elderly nursing home residents accounted for 30-70% of COVID-19 deaths in high-income countries during the first wave, despite comprising <1% of the population. [7] The IFR for COVID in the elderly (people 70 and older) who live in the general community (i.e., not in a nursing home setting) was 2.4% (range 0.3%-7.2%), while the IFR for elderly overall was 5.5% (range 0.3%-12.1%). [7] The IFR is highest in people >85 years, especially if co-morbidities are present. [7] The IFR for all elderly people would be expected to be lower than just mentioned (perhaps much lower), if prompt, excellent outpatient and inpatient treatment were routinely provided (see Question 3) and if appropriate measures are instituted to protect the vulnerable from exposure.

Ioannides has concluded (as Fauci, et al, had initially suggested might be the case [2]) that the IFR of the original SARS-CoV-2 virus is comparable to that of particularly severe influenza viruses (i.e., <0.2%). [3, 4, 6, 7, 8] There is disagreement on this issue, however. [9-10] Some contend that it is inaccurate, misleading, and reckless to claim that the IFR of SARS-Co-V-2 is comparable to that of a severe influenza virus. [10] One reason for the controversy is that the IFR determinations for these two viral infections have been based on different methods of data collection. [9] Furthermore, the data collected has often been of sub-optimal scientific quality (see Articles #3, #4, #15, and #16 on website).

In support of the notion that the deadliness of the original SAS-CoV-2 virus has been comparable to that of a particularly severe influenza virus is the fact that during the 5-month duration 2017-18 seasonal influenza epidemic (which was a flu season of above average severity that most of the public does not remember), 641 children died of influenza (in the USA) [11], while during the first 18 months of the COVID epidemic 470 children have died of COVID in the USA. [12]

As with other questions addressed in this article, it would seem wise to convene an independent international panel of fairly selected, eminent epidemiologists and virologists to respectfully, thoroughly, objectively, transparently, and publicly examine epidemiologic studies of SARS-CoV-2 and try to resolve disagreements as to whether the IFR of the original SARS-CoV-2 virus was and is comparable to that of severe influenza, or not. It is neither fair, nor healthy, to leave the public in a suspended state of confusion and contentious disagreement on this issue.

Overall, Dr. Ioannides’ conclusions have seemed to hold up well to scientific scrutiny. Until recently, COVID has posed relatively little threat to children and people under 60. There is legitimate concern, however, that, if we are not careful, SARS-CoV-2 could become a major threat to children and all adults (see Questions 7-11 and 13).

COVID-19 is potentially serious and fatal: Dr. Ioannides’ data and conclusions do not mean that COVID, to date, has not been a potentially serious and fatal illness. Both influenza and COVID can be fatal, and both must be taken very seriously by the medical community and the public. During the 2017-18 influenza epidemic 61,000 people died of influenza in the USA, over a period of 5 months. [11] As of this writing, it has been stated by the CDC that 633,785 people have died from COVID in the USA, over a period of 18 months. [12] However, it must be appreciated that the criteria that have been used to declare a “COVID death” have not been scientifically sound (they have been excessively broad and non-uniform), and COVID diagnoses have been based on misuse of the PCR test (see Question 5). (Also, see Articles #3, #4, #15, and #16 on the website for further details and references.) This has resulted in our not knowing what percentage of the 633,785 “COVID deaths” have truly been deaths due to COVID. Sadly, due to lack of scientific rigor and discipline, we simply do not know how many people have truly died of COVID. We also do not know how many of the true COVID deaths could have been prevented with appropriate outpatient and inpatient treatment (See Question 3).

Unusual, worrisome clinical features of COVID-19: Although the Infection Fatality Rate (IFR) of the original SARS-CoV-2 virus appears to be comparable to seasonal influenza of above-average severity, there certainly have been several frightening and unusual clinical features of COVID that have appropriately worried those on the medical front lines, particularly ICU physicians. [13] For one thing, abnormal clot formation has seemed to be more common in COVID than in influenza epidemics. [14, 15] Also, COVID has seemed to more frequently and severely affect organs outside of the respiratory tract, including the brain and heart. [16-24] The frequency and severity of loss of smell and taste has also seemed distinctive and unusual. [25] Despite these worrisome features, it is heartening to note that the IFR for COVID has, nevertheless, appeared to be comparable to that of above-average seasonal influenza—at least up until now.

 

2. Although the virulence (deadliness) of the original SARS-CoV-2 virus has not appeared to be greater than that of an above-average influenza virus, is that still the case today? Is the Delta variant more lethal than its predecessors? Might future variants be more deadly?

Fortunately, current epidemiologic data suggest that the Delta variant is not more virulent (deadly) than its SARS-CoV-2 predecessors. [6, 7, 26] Despite a current predominance of the Delta variant in England, recent data from Public Health England suggest that the mortality rate for COVID is still 0.2%, at least in the unvaccinated. [26] However, some very experienced and accomplished ICU physicians on the front lines have a strong impression that the Delta variant is more dangerous than the original SARS-CoV-2 virus and previous variants. [27] If this impression is accurate, it raises the question of whether more severe illness with the Delta variant is truly due to increased intrinsic virulence of this variant or is due to vaccine-induced ADE (Antibody Dependent Enhancement) (see Question 8), or both. In this regard, it is important to note that the Public Health England data revealed a higher mortality rate (0.96%) among the fully vaccinated, compared to the unvaccinated (0.2%). [26] Additional scientifically sound study of the intrinsic virulence of the Delta variant (and future variants) and of the occurrence of ADE phenomena are greatly needed.

Even if the Delta variant is not more virulent than its predecessors, some scientists have raised concern that the current mass vaccination campaign will eventually generate more deadly variants in the future (see Questions 7, 9, 11, and 13 for further discussion and references.) Even if future variants are not more intrinsically deadly, we need to be concerned about the possibility that vaccinated people may be at particular risk for dangerous vaccine-mediated enhancement of disease severity (ADE phenomena) when they are eventually exposed to current and future variants, regardless of the virulence of those variants—an issue that will be discussed in greater detail later (see Question 8.)

Furthermore, during the current surge of worrisome hospitalizations that is being attributed to the Delta variant, it will be important to determine what percentage of these hospitalized patients are truly suffering from SARS-CoV-2 infection (with its disease-causing spike protein) and what percentage are suffering, instead, solely from adverse effects of the COVID vaccines (due to the spike protein production being induced by the vaccines). See Question 10 for further explanation of this issue. And it will be important to determine what percentage of hospitalized patients with true SARS-CoV-2 infection have developed their infection, in part, from temporary vaccine-induced immunosuppression (see Question 10).

The above complexities and concerns are discussed in more detail in Questions 7-11 and 13. Those discussions provide further references. As with the other questions raised in this article, it would be helpful to have an “Independent International COVID Commission” examine and try to develop consensus regarding Question 2.

 

3. Are treatments available that can prevent serious COVID illness and COVID deaths?

Fortunately, yes.

Inpatient treatment of severe COVID illness: Although COVID has the potential to cause severe illness and death, excellent treatments are available for severe illness and, if optimally used, can prevent many deaths. [28-47] (See Articles #5 and #14 on the website for further details and references regarding treatment)

COVID is a two-phase illness. [48-65] The first phase is the “viral phase,” which lasts approximately 7-10 days. It is during this phase that the virus rapidly replicates (particularly during the first 5-7 days), causes flu-like respiratory symptoms, and is infectious. The second phase is the “immune reaction phase,” which starts during the latter part of the first week and continues for 2-4 weeks, reaching a peak during the 2^nd and 3^rd weeks.

Most people who develop severe life-threatening COVID illness and end up in the hospital or ICU do so because they experience an excessive immune reaction phase—a dangerous and harmful “hyperimmune reaction.” Their immune system has excessively over-reacted to the virus and this over-reaction (and/or dysfunctional reaction) causes life-threatening inflammatory damage to the lungs and other organs. These patients are at high risk of dying, not because of ongoing viral infection, but because of an unusual hyperimmune reaction to the virus.

Fortunately, this “hyperimmune reaction” (which includes, but is not limited to “cytokine storm”) can be successfully treated, if appropriately aggressive immunosuppression is promptly and proactively provided (e.g., appropriate use of corticosteroid and anti-cytokine therapies). [28-47] These treatments have been available for many years. Failure to treat such patients with prompt appropriately aggressive immunosuppression often results in death.

Early outpatient treatment of COVID: In addition to excellent inpatient treatments for severe COVID, there are outpatient treatments that have potential to subdue the viral phase, so that severe COVID illness is less likely to evolve. [27, 66-83] Oral outpatient medications can impair viral replication and, thereby, reduce viral load and disease severity. For example, a growing body of evidence has suggested that prompt initiation (at onset of symptoms) of hydroxychloroquine plus azithromycin, or ivermectin plus azithromycin, plus nutraceuticals (e.g., zinc, vitamin D, and vitamin C) might reduce likelihood of hospitalization and death by as much as 85% and 75%, respectively. [74, 75] More than 200 studies support the use of hydroxychloroquine in the early treatment of COVID. More than 60 studies, including randomized trials, support the use of ivermectin in the treatment of COVID. Ivermectin has become an apparently successful first-line treatment in many countries around the world, most notably in India. Hydroxychloroquine, azithromycin, and ivermectin appear to be quite safe and very helpful. They have not deserved the unfair and unscientific demonization and belittling they have received, nor have their prescribers and researchers. There is very little to lose with these outpatient treatments and most likely a considerable amount to gain.

In addition to the viral phase and the immune reaction phase there is a third potential aspect of COVID illness that needs recognition and proactive treatment—namely, abnormal clotting (thrombosis) within large, medium, and/or small vessels—particularly the small vessels in the lungs. [14, 15, 83] This abnormal clotting is largely triggered by the viral spike protein and can begin during either the viral phase or the immune reaction phase. (See Question 10 for further details and references.) Fortunately, this clotting problem (which may be accompanied by spike protein-induced, immune-mediated microvascular endothelial injury and resultant partial microvascular occlusion) can be either prevented or successfully treated with timely administration of anticoagulation.

We are very fortunate that the above inpatient and outpatient treatments are available—especially the treatments that can prevent or minimize severe COVID illness. By preventing damage, these treatments may also be capable of minimizing development of “long COVID.”

 

4. If the SARS-CoV-2 virus is not more deadly than an above-average influenza virus, why have we seen scenes of overwhelmed ICUs and refrigerated trucks full of dead bodies?

This is an important and complex question. Multiple factors have been involved. [84] (Also, see Article #17 on the website). One factor, as already emphasized, is that COVID can certainly be fatal, particularly if it is not treated promptly and appropriately. Severe COVID illness and COVID death will be much more common if prompt outpatient treatment of the viral phase is not provided and/or if prompt appropriately aggressive treatment of the hyperimmune phase is not provided and/or if anticoagulation is not promptly provided (when indicated), as discussed above. Unfortunately, since onset of the pandemic, these treatments have been strongly discouraged by those in charge of the COVID pandemic [27, 85-88], and this has probably led to unnecessary deaths and residual damage, as well as preventable ICU admissions and prolongation of hospitalizations.

 

It is unclear what percentage of patients who have truly died from COVID had received prompt and optimal outpatient and/or inpatient antiviral therapies (during the viral phase of COVID) and had received prompt and optimal immunosuppressive therapies (during the hyperimmune phase) and had received prompt and appropriate anti-coagulation (when indicated). It is very possible that most of those who have died of COVID did not receive prompt and optimal treatment. Unfortunately, quality data on this issue have not been adequately collected.

Several other factors have contributed to the frightening media images and anecdotes associated with COVID. [84] Please see Article # 17 (on the website) for a detailed discussion of multiple factors (besides the virus itself) that have played a role in creating the impression that the COVID pandemic is far more serious than an above-average influenza epidemic—despite the infection fatality rate being comparable. It is important to ask, has the main problem been the deadliness of the virus, or has deadliness of the health care delivery system and deadliness of certain COVID policies also played a major role?

It is also appropriate to ask whether deliberate efforts have been made to psychologically manipulate the public into embracing a particular narrative and impression. To achieve a particular goal, have applied behavioral psychology techniques been used to create excessive fears, anxiety, chaos, confusion, mystification, cognitive dissonance, division, intolerance, extremism, and anger—at the expense of careful examination and healthy dialogue?

 

5. Why have there been so many “cases” of COVID?

Since the beginning of the pandemic, the public has been inundated with frightening daily reports of total cumulative “cases of COVID.” However, these case counts have been based on misused PCR tests and scientifically unsound definitions of a “COVID case,” as discussed in detail in Articles #3, #4, #15, and #16 on the website. Unfortunately, the CDC has used an inappropriately high Ct cut-off for determination of a positive COVID PCR test. Instead of using a Ct cut-off of 26, or 30, the CDC has used a cut-off of 40, 45, even 50. This has resulted in a high number of false positive results, or at least inadequately interpretable results. [89-112]

Compounding this problem, the CDC has considered any person with a “positive” COVID PCR test, even if positive only after 45 cycles (i.e., at a Ct of 45) and even if asymptomatic, to be a “new case of COVID.” This is not a scientifically sound way to collect data on new cases of COVID. Furthermore, it is unclear whether the specificity of the COVID PCR test is as great as claimed by the lab manufacturing companies. Sadly, we do not know how many true cases of COVID have cumulatively occurred since the onset of the pandemic—just as we do not know how many true COVID deaths have occurred. It is not too late to finally start collecting data in a proper, scientifically sound fashion (including using genome sequencing, rather than relying solely on the current PCR tests).

 

6. How could the COVID pandemic have been managed in the USA had no vaccines been available? What would have been done and what would have happened?

Fortunately, the human immune system (HuIS) normally has tremendous capacity and uses great wisdom to deal with viral infections, including those as threatening as SARS-CoV-2. [113-132] According to the initial COVID narrative, SARS-CoV-2 was brand new, the HuIS had no experience with it, and the HuIS would, therefore, have great difficulty handling it. That is not true. The HuIS’s extensive experience with past coronaviruses prepared the HuIS to deal quite effectively with the SARS-CoV-2 virus, at least in the vast majority of instances. [113-132]

The following is general knowledge among experienced virologists and epidemiologists: The HuIS wisely approaches viruses, including SARS-CoV-2, in multiple ways. (See Article #7 on website.) It does not simply and only produce antibody to a single major component of the virus, like the spike protein. It produces antibodies to multiple components up and down the virus. The HuIS uses all of its dimensions (all of its innate immunity tricks and all of its adaptive immunity tricks, including memory T and B cells) to create robust, durable natural immunity against the virus. Natural immunity to SARS-CoV-2 is far superior to vaccine-induced immunity and is far more durable. [113-132] The people who are currently best protected from COVID, including future variants, are those who have already had SARS-CoV-2 infection and have developed natural immunity to it.

In the absence of a COVID vaccine, a considerable percentage of the population would have become infected with the SARS-CoV-2 virus and would have developed natural immunity to it. Realistically, as well as preferably, the relatively young (people under 60) and healthy people would be the largest group that became infected, because they would be the most exposed and the most able to withstand the infection without harm, and almost all of them would do well (see next 3 paragraphs). Infection of this group, and the natural immunity resulting from that infection, would then serve to increasingly protect the elderly and vulnerable. Common sense public health mitigation measures would be used to further protect the elderly and most vulnerable.

In addition to relying on natural immunity provided by the HuIS, all people who did become symptomatically infected with COVID would have been started on outpatient anti-viral therapies (according to their individual needs) as soon as it was apparent that they were having symptoms of COVID. Such patients would be promptly started on a combination of medications that would be likely to at least somewhat slow viral replication (e.g., hydroxychloroquine and azithromycin, or Ivermectin and azithromycin) plus nutraceuticals to support the HuIS (e.g., vit D, vitamin C, Zinc). Those who appeared to have an unusually large and/or threatening viral load (which could be estimated by the Ct values at which their serial COVID PCR tests were positive), or were otherwise at higher risk, could, in addition, be promptly treated with monoclonal antibodies. If a patient’s serial studies for d-Dimers were positive, early outpatient treatment with anticoagulation (e.g., oral apixaban) could be initiated. In addition, patients would be placed on outpatient O2 monitoring with a finger probe, to detect early signs of worsening. These efforts have been shown to significantly reduce the likelihood of early infection evolving into worse illness that would require hospitalization. [74, 75]

If a patient who is receiving the above outpatient treatment shows signs of worsening despite that treatment, prompt evaluation for presence of a hyperimmune response would be initiated and the patient would be hospitalized, if necessary. If evidence of a hyperimmune reaction is found, the patient would be treated promptly with appropriately aggressive immunosuppression, including corticosteroid and anti-cytokine therapies, as already discussed. (Also, see Articles #5 and #14 on website.) The need for anticoagulation would also be addressed, both during the viral phase and the immune reaction phase.

With the above prompt outpatient treatment of early illness and with prompt, appropriately aggressive treatment of those who develop severe illness (due to a hyperimmune reaction), a high percentage of the hospitalizations and deaths that have occurred during 2020 and 2021 would likely have been prevented.

Meanwhile, in the absence of vaccination, the virus and the HuIS would work together to arrive at a mutually acceptable compromise—whereby the virus might be allowed to live peacefully within the human being, as long as it stays under control and does not cause regrettable harm. Under such natural circumstances (i.e., without vaccination interference) the virus normally and naturally mutates in a benign direction. That is, the virus gradually becomes less and less virulent, less dangerous. The virus might become a little more transmissible, but that would be acceptable if it has become less virulent. If at any time the virus starts to get out of control, the HuIS would quickly re-establish the upper hand. The HuIS is tolerant, but strict. That is how epidemics (due to viruses with IFRs in the range of COVID and influenza) are expected to play out, naturally, in the absence of vaccination. (See Article #18 on the website.)

The end result of the above process is that considerable herd immunity develops, which protects everyone; in the meantime, the above treatments minimize hospitalizations and deaths; and the epidemic subsides within several months.

As with ecology and protection of the environment, it is best, if possible, to not interfere with nature, including natural immunity. Like ecosystems, the human immune system is a complex, delicately-but-ingeniously balanced system that does very well when left alone. As with ecosystems, human interventions, even if well-meaning, particularly when arrogant and hubristic, can tip balances and cause dreadful unintended consequences. We need to keep this in mind when we intervene with certain types of vaccines. Ecologists and environmental activists know this.

 

7. What happens when an epidemic like the COVID pandemic is primarily treated with a mass vaccination campaign, using the currently available sub-optimal COVID vaccines?

If an optimal vaccine (meaning the vaccine completely prevents infection and transmission) were available for COVID and were safe, use of such a vaccine for the most vulnerable would clearly be helpful.

However, historically, virologists and vaccinologists have not been able to develop a safe, optimal vaccine for coronaviruses or respiratory syncytial virus (RSV). [133-140] Over the past 20 years the best they have been able to do is develop a sub-optimal vaccine—meaning that the vaccine might reduce disease severity somewhat but does not adequately prevent infection or transmission. Those sub-optimal vaccines have not proven to be adequately effective or adequately safe. In fact, animal studies of these previous coronavirus vaccines have shown them to be dangerous, primarily because of antibody-dependent enhancement (ADE) of viral replication and disease severity within the vaccinees. [133, 134, 138-140] (See Question 8 for further discussion of ADE.)

Despite the above history of coronavirus vaccine failures, the current COVID pandemic has been primarily managed with roll out of a rapid, massive vaccination campaign, using sub-optimal uni-dimensional vaccines (directed at only the spike protein), in the midst of the active pandemic and in the midst of considerable lockdown measures. According to many eminent, experienced, caring, virologists/vaccinologists (including, most notably, Dr. Geert Vanden Bossche), this type of vaccination campaign is a recipe for disaster. [141-150] Why? Because, according to these scientists, the sub-optimal vaccine inadequately prevents the virus from entering cells, replicating in those cells, and being transmitted to other people. When the virus replicates in the vaccinated person’s cells, new mutations develop (resulting in new “variants of concern”) that would not have developed in the absence of the mass vaccination program. These new mutations confer the new variant with an ability to “escape” the vaccine-induced anti-spike protein antibody. As a consequence, the vaccine-induced antibodies quickly become less effective and the new variant more easily enters cells, more easily replicates, and tends to be more transmissible than its predecessors. Some vaccinologists/pharmaceutical companies might try to counteract this phenomenon by producing a new, “updated” vaccine against the latest mutated spike protein, but it is impossible to keep up with the new escape mutations that inevitably evolve.

For further discussion, details, and references, regarding the concerns of Dr. Vanden Bossche and those who agree with him, please see his website: https://www.geertvandenbossche.org

Initially, the main concern about the mass vaccination campaign was the potential development of increasingly reduced vaccine efficacy and increased viral transmissibility. But another huge concern is potential eventual development of a vaccine-created new variant that is far more virulent (deadly) than any of its predecessors—which, fortunately, has not yet been well documented to have happened. That deadly virus would be a threat to both the unvaccinated and vaccinated. In fact, such a virus would be a greater threat for the vaccinated, because of ADE (see Question 8).

Although Dr. Vanden Bossche and many other eminent scientists are deeply worried about the above concerns, and may be correct, others (Dr. Michael Yeadon, e.g.) disagree and are not fearful of new variants. Please see Dr. Yeadon’s article (and other articles of interest) on the PANDA (PANdemics Data and Analytics) website: https://www.pandata.org/how-broad-is-covid-immunity/

Also, please see Question 9 for further discussion of Dr. Yeadon’s point of view.

It would be very wise and helpful to assemble an expert panel of fairly selected, internationally respected virologists and vaccinologists to carefully, critically, respectfully, transparently, and publicly examine this issue. Indeed, Dr. Vanden Bossche, in an open letter to the global medical community, pleaded (many months ago) for just that. Such dialogue and careful examination is fundamental to Medicine and Science but has been largely absent during the COVID pandemic. Instead, we have seen intolerance of challenges to the prevailing narrative. Dr. Vanden Bossche’s plea for healthy dialogue has gone unheeded, so far.

 

8. What is ADE (Antibody Dependent Enhancement) and how does it affect vaccinated individuals?

The concept of ADE is complex and incompletely understood. [151-179] Moreover, the extent to which ADE will complicate the COVID pandemic is unclear and remains to be seen. As with Question 7, it would be wise to assemble an expert panel of fairly selected, internationally respected virologists and vaccinologists to carefully, critically, respectfully, and publicly examine this issue. As part of informed consent, the public certainly deserves to know and needs to know the extent to which vaccine-induced ADE is or is not likely to occur after COVID vaccination.

ADE is a phenomenon that occurs in delayed fashion after some vaccinations for some viruses. Those viruses include SARS-1, MERS, feline infectious peritonitis virus (a feline coronavirus), RSV, dengue, Ebola, some influenza viruses, and probably SARS-CoV-2. A more accurate and helpful term for ADE might be “immune-mediated (or vaccine-induced) enhancement of viral replication and disease severity.” When the inadequately neutralizing antibodies that are produced by sub-optimal vaccines (like the COVID vaccines) bind to the virus, this antibody-virus complex has potential to do harm via one or both (and possibly other) of the following ADE mechanisms:

Vaccine-induced enhancement of viral replication: The antibody-virus complex can, paradoxically, enhance entry of the virus into certain human cells, most notably macrophages, where the semi-protected virus (because it is coated with antibody and acts kind of like a Trojan horse) can prevail within the macrophage and rapidly and massively replicate and spread within the vaccinated person. This can then trigger an eventual dangerous explosive hyperimmune reaction, including cytokine storm. The huge number of newly replicated viruses not only threaten the vaccinated person but can be spread by the vaccinated person to others, including both the unvaccinated and vaccinated. In that sense, the vaccinated people, ironically, become relative “super spreaders.”

Vaccine-induced enhancement of immune reactivity: Even in the absence of enhanced entry of virus into macrophages, the antibody-virus complex can trigger excessive cytokine cascades, complement-mediated inflammatory reactions, and/or killer T-cell reactions that result in dangerous levels of inflammation and immune-mediated injury.

Resultant vaccine-induced enhancement of disease severity: When one or both of the above phenomena occur, the end result is worse disease severity (in the vaccinated person) and worse spreading of the virus (by the vaccinated person).

The above ADE phenomenon, if it truly occurs with SARS-CoV-2, is particularly likely to occur when vaccinated people encounter the SARS-C0V-2 virus (any variant) 5-6 months (or longer) after their vaccination. When they encounter the virus at that point, they are at risk of experiencing this dangerous, life-threatening hyperimmune reaction to the virus, even if the virus is not particularly virulent. This ADE phenomenon primarily applies to the vaccinated, not the unvaccinated.

Since most people were vaccinated less than 6 months ago, we are only now in a position to find out the extent to which ADE is a problem with these COVID vaccines. The clinical trials were much too short to evaluate this issue.

It was predictable that ADE might prove to be a problem with the COVID vaccines, because ADE was noted to occur in trials of vaccines against other coronaviruses, as well as RSV, Dengue, and Ebola. Indeed, attempted vaccines against SARS-1 were quickly abandoned because life-threatening ADE phenomena (upon later exposure to the wild virus) were common.

So, there are legitimate concerns that COVID vaccinated people may well contribute to the development, incubation, and shedding of more transmissible and potentially more lethal variants (if Dr. Vanden Bossche is correct) of the SARS-CoV-2 virus. If so, the vaccinated people would, thereby, put unvaccinated people (including children) and other vaccinated people at increased risk of becoming infected, potentially with a more lethal and vaccine-resistant strain. And, even with less lethal strains, vaccinated people (much more so than unvaccinated people) might be at risk of experiencing dangerous ADE-mediated hyperimmune reactions when they are later exposed to the wild virus.

The above vaccine-created problems would not occur without a rapid massive vaccination campaign with sub-optimal vaccines. Natural immunity does not result in increasingly virulent strains of the virus, nor is it expected to cause ADE-mediated hyperimmune reactions. As already discussed under Question 7, when a pandemic is not treated with massive vaccination the virus mutates in a benign direction, with mutations developing that render the virus less lethal and better able to live relatively peacefully within humans. The concern of many eminent scientists is that vaccines like the COVID vaccines may do the opposite (generate more worrisome variants) and predispose vaccinated people to dangerous ADE when/if they later encounter the virus.

In addition to ADE phenomena, there is another conceivable side effect of mass vaccination with a sub-optimal vaccine. Some vaccinologists are concerned that such vaccination might significantly impair/dysregulate natural immunity (e.g., impair natural antibodies), rendering the vaccinee (at least temporarily) less able to handle not only COVID but other viruses. [180-182] The extent to which this is true is unclear and warrants thorough healthy dialogue among experts in the field.

 

9. What is most responsible for the new more worrisome “variants of concern”—the unvaccinated people or the vaccination campaign? Or is it incorrect to state that “variants of concern” represent a true threat?

The prevailing narrative: According to the CDC, the White House COVID Task Force, the NIH, their adherents, and the conventional news media, the USA is currently in the midst of an “epidemic of the unvaccinated.” The message is that new “variants of concern” have been developing because of the people who have not become vaccinated. According to this narrative, the unvaccinated people frequently become infected; this allows greater opportunity for the virus to replicate and mutate within those people; new more worrisome variants develop; then these unvaccinated people spread the new variants to other people, including some who have been vaccinated.

The further claim is that during the summer of 2021 “more than 99% of hospitalized cases of COVID in the USA are unvaccinated people.” However, the accuracy of these data is unclear. Unfortunately, COVID-related data collection in the USA (e.g., the diagnostic and classification criteria used) has been of such low scientific quality that the data cannot be taken at face value and must be challenged. These data are certainly at odds with data from Israel, England, and other countries (see Question 11 and the Note below). The prevailing narrative claims that if everyone were to become vaccinated, the virus would no longer have opportunity to replicate and mutate, new variants of concern would not emerge, and the pandemic would largely subside.

The above narrative might be accurate, if the vaccines were optimal, rather than sub-optimal.

Note: Regarding the statement that “99% of hospitalized cases of COVID are comprised of unvaccinated people,” the CDC has defined “unvaccinated” as anyone who has either received no COVID vaccines; received only one mRNA vaccine; or has received two mRNA vaccines but is less than 14 days out from their second shot. So, those who are partially vaccinated, including those who have received 2 shots but are less than 14 days past their second shot, are considered “unvaccinated” and lumped in with those who have received no COVID vaccination.

It is important to know that the mRNA vaccines, themselves, can temporarily suppress the immune system, particularly in older persons. That is a potential cause of elderly people contracting and dying of COVID shortly after their first (usually) or second (sometimes) dose of the mRNA vaccine—in which case, according to the CDC, their death would represent a COVID death in an “unvaccinated” individual, because they were not 14 days out from their second vaccine dose.

The counter-narrative: According to other eminent scientists, it is the sub-optimal vaccines that are responsible for the emergence of new “variants of concern.” (See Geert Vanden Bossche website.) They contend that the “variants of concern” are emerging because of the massive vaccination campaign, not because of the unvaccinated. In their view, the vaccinated population is generating the new variants of concern that then threaten both the unvaccinated and the vaccinated, including children. And it is the vaccinated who become the predominant spreaders of new more worrisome variants. And, if/when a new variant emerges that is particularly deadly, it will be the mass vaccination campaign that is responsible.

According to this counter-narrative (best explained by Dr. Vanden Bossche), we are currently in the midst of a vicious cycle—one created by the mass vaccination campaign—that is generating new variants that have the potential to increasingly threaten everyone, including children The only way to break this vicious cycle, before it is too late, is to immediately shut down the vaccination campaign. Instead, a doubling down on vaccination is being advocated by supporters of the prevailing narrative, including a third booster and vaccination of children. According to the counter-narrative, this represents poor science and mis-guided, dangerous policy.

To review: There are two categories of mutations (variants): a) mutations that normally emerge in the absence of a mass vaccination campaign and b) mutations that emerge under the pressure of a mass vaccination campaign with sub-optimal vaccines, during an active pandemic. The first type of mutations are fully expected and are no cause for alarm—they evolve in a benign direction and are easily managed by the natural, unimpeded immune system. It is mutations that emerge under the pressure of a mass vaccination campaign with sub-optimal vaccines that some scientists (e.g., Geert Vanden Bossche) think have potential to become worrisome. Incidentally, excessive lockdown adds to this pressure on the virus to mutate in a worrisome direction.

According to the counter-narrative, the new “variants of concern,” are being caused by the massive vaccination campaign, not by the unvaccinated—because these vaccines (as well as excessive lockdown) put abnormal (un-natural) pressure on the virus to mutate in ways that enable it to “escape” the narrowly focused vaccine-induced antibodies, which means that each edition of the vaccine soon becomes obsolete, requiring a new edition of the vaccine, which will in turn quickly become obsolete.

Furthermore, according to Dr. Vanden Bossche, the new variants produced by the vaccination campaign tend to become more transmissible and have potential to eventually become more lethal. The eventual more lethal variants (created by the vaccine) would be a huge threat to both the vaccinated and the unvaccinated, including children, and the deaths that occur will be due to the vaccination campaign, not the unvaccinated. As that more lethal variant situation develops, it will be the vaccinated people who will be the predominant “spreaders” of this more lethal variant, because vaccine-induced variants incubate and replicate (even highly so) within the vaccinated. According to this counter-narrative, the unvaccinated, ironically, will need to try to protect themselves from the vaccinated, who carry and spread the more lethal variant.

So, according to this counter-narrative, the current COVID situation is not an “epidemic of the unvaccinated” that threatens the vaccinated. It is the opposite. It is an epidemic that has been perpetuated and made worse by the vaccination campaign. It is an “epidemic of the vaccinated” that now threatens all of Humanity, including the vaccinated, including children. And this would not have happened in the absence of a mass vaccination campaign with a sub-optimal vaccine.

This counter-narrative is concerned that we will likely soon see increasing numbers of true COVID cases, hospitalizations, and deaths—involving the vaccinated as much, or more, than the unvaccinated. Because of ADE, the vaccinated will be more likely than the unvaccinated to experience more severe illness and death.

There is, however, a second, different counter-narrative, one advanced by Dr. Michael Yeadon: https://www.pandata.org/how-broad-is-covid-immunity/

Dr. Yeadon does not think any of the current or future new variants are or will be more virulent than the initial SAR-CoV-2 virus, regardless of whether those variants develop in the absence or presence of a mass vaccination campaign. He is not concerned about variants that inevitably develop in the absence of vaccination; nor does he agree with Dr. Vanden Bossche’s concern that mass vaccination will eventually and inevitably produce a more virulent variant. With or without mass vaccination, Dr. Yeadon believes that new variants will become increasingly less virulent and, thereby, less threatening. He thinks it is incorrect to fear and create public alarm about new “variants of concern.” Regarding “variants of concern,” he disagrees with both the prevailing narrative and the Vanden Bossche narrative.

Both Dr. Yeadon and Dr. Vanden Bossche feel strongly, though, that the mass vaccination campaign be immediately halted, but for different reasons. Dr. Vanden Bossche worries that continued vaccination will eventually create a catastrophically virulent variant. Dr. Yeadon thinks the vaccination campaign (including its promotion of worries about new variants) should be immediately halted because it is unsafe, unnecessary, and stokes unwarranted and harmful fears.

Which narrative is correct? Is the prevailing narrative, the Vanden Bossche counter-narrative, or the Yeadon counter-narrative, correct? This is obviously an extremely important and urgent question. As with Questions 7 and 8, it would be wise to assemble an expert panel of fairly selected, internationally respected virologists and vaccinologists to carefully, critically, respectfully, and publicly examine this issue. As part of informed consent, the public certainly deserves to know and needs to know the extent to which the massive vaccination campaign, or the absence of vaccination, is or is not driving emergence of increasingly worrisome variants. The public needs to know whether they need to fear “variants of concern” or not.

Personally, I suspect (and I certainly hope) that Dr. Yeadon is correct—that we need not fear current or future “variants of concern.” I do think, however, that Dr. Vanden Bossche’s concerns are legitimate, need to be taken very seriously, and must be thoroughly examined and discussed. I think the prevailing narrative (that this is a “pandemic of the unvaccinated”) is definitely incorrect—scientifically and ethically.

Another reason that COVID-related hospitalizations and deaths could increase in the months ahead is that increasing numbers of vaccinated people may experience serious vaccine-related adverse effects that require hospitalization and may cause death. (See Question 10.) Such hospitalizations and potential deaths will not be due to actual SARS-CoV-2 infection, but, rather, to COVID vaccine side effects.

 

10. In addition to the above concerns are there other concerns about the COVID vaccines?

Many eminent scientists and many physicians are deeply concerned that the COVID vaccines are not nearly as “safe” as has been claimed and, in fact, are quite dangerous and unwise (at both the individual and population levels)—as already mentioned above and further explained below (and in articles posted in notesfromthesocialclinic.org). (See Articles #6, #7, and #9-12 on the website.)

The two available mRNA vaccines (Pfizer and Moderna) are lipid-nanoparticle-formulated, nucleoside-modified mRNA vaccines that encode the receptor-binding domain of the spike glycoprotein of the SARS-CoV-2 virus.

The mRNA vaccines work by entering human cells and directing them to produce the spike protein. Once those cells produce the spike protein, the spike protein ends up sitting on the outside of the cell wall, where it is recognized by the immune system as an unwanted foreign substance. The immune system then produces antibodies against the spike protein and directs killer T cells to destroy the cells that have produced the spike protein. To an unknown extent, some of the spike protein breaks free and circulates through the bloodstream, before it becomes neutralized by the antibody.

Historically, during the development of mRNA technology, two major problems became apparent—unmodified mRNA is too immunogenic (stimulates the immune system too much) and too unstable to be clinically feasible [183]:

Unmodified mRNA proved to provoke a degree of immune reaction that rendered it unfeasible for clinical use. [183] For example, by stimulating Toll-receptors, unmodified mRNA adversely activates cells of the innate immune system and increases production of type 1 interferon and pro-inflammatory cytokines. It became necessary to modify the mRNA so that it would be less immunogenic. This was accomplished by incorporating pseudouridine into the mRNA. This nucleoside-modified mRNA proved to not only suppress unwanted mRNA-mediated immune activation, but also enhanced the stability and functionality of the mRNA.

A potential problem with nucleoside-modified mRNA is that it apparently is less immunogenic because it dampens innate immune sensing. This suggests that it might be at least transiently immunosuppressive when injected into humans. This, in turn, raises the possibility that some people who receive the vaccine may develop at least a transient and possibly clinically significant decrease in immune competency shortly after vaccination. Indeed, in a phase I/II study of COVID-19 vaccine, healthy volunteers (under age 56) developed a transient, dose-dependent lymphopenia during the first few days after initial vaccination. [184] Whether interferon and cytokine levels also dropped is unclear, because this was apparently not studied (or at least not reported). These data raise the possibility that some elderly people, who may already be relatively less immunocompetent, may not tolerate this transient immunosuppression as well as younger, healthier people—i.e., the immunosuppression may be less transient and/or more clinically significant. It is conceivable that this could predispose some elderly people to develop a post-vaccination infection (by whatever infectious agents happen to be around).

So, one concern about the mRNA vaccines is that these vaccines may cause a transient immunosuppression that could render elderly people transiently more vulnerable to becoming infected (with whatever bacteria or virus they may be exposed to). It is possible, for example, that some of the deaths reported in some nursing homes after mass vaccination could be due to people dying from any one of a number of infectious agents because of transient vaccine-induced immunosuppression. After all, alert innate immune sensing, type 1 interferon, cytokines, and lymphocytes play major roles in our initial immune defense against infection.

Although eventual studies may prove that there is little or no need to be concerned about the above, this issue has not yet been adequately studied.

A second problem with the mRNA technology is that unmodified mRNA is normally quickly digested, before it has a chance to instruct the ribosomes to synthesize the desired protein (spike protein in the case of the COVID vaccine). So, to make the technology clinically feasible, the mRNA must be protected from digestion. This is done by encapsulating the mRNA in a lipid-nanoparticle. The lipid is polyethylene glycol (PEG). The lipid encapsulation protects the mRNA from digestion, makes it more stable, and enhances its entry into the cytoplasm of cells. [183]

This raises the following unanswered question: Since it is protected, how long does this PEG-encapsulated mRNA remain in our cell’s cytoplasm before it eventually disintegrates? Does it persist for just hours, or for days? weeks? months? Do we know? This is important, because if the mRNA continues to instruct the ribosomes to make spike protein only for a matter of hours or days, this might be reasonable. But if the PEG-encapsulated mRNA persistently instructs the ribosomes to keep making spike protein for weeks and weeks, this might create prolonged and harmful (not to mention unnecessary) immune reactions to this prolonged production of spike protein. [185] In this way could the vaccine be predisposing some people to chronic immune reactions?

This raises a third concern. We want a vaccine to provoke an appropriate immune reaction for an appropriate length of time. We do not want to provoke an excessive reaction or, a reaction that persists for an excessive length of time. It is unclear whether the mRNA vaccines provoke only an appropriate reaction (i.e., an appropriate level of antibody production, not too high or too low) and only for an appropriate length of time. Although eventual studies may prove that there is little or no need to be concerned about the above, this issue has not yet been adequately studied.

A fourth concern: How healthy is it to have PEG-encapsulated mRNA sitting in the cytoplasm of our cells? Do we know with certainty which cells of the body receive the vaccine’s PEG-encapsulated mRNA? Is it just the muscle cells near the site of injection? Does the PEG-encased mRNA enter all cells that have a lipid cell membrane, including brain cells, heart cells, ovarian cells? Probably so. Do we know the consequences of housing PEG-encapsulated mRNA in our various cell types?

It turns out that the mRNA does not just stay in the arm that has been jabbed. According to rodent studies that were conducted by Pfizer but were provided only upon the insistence of the Japanese government, the mRNA (or at least the lipid nanoparticle) gets into the regional lymph nodes, then the general circulation, and enters the cells of many organs, including the liver, spleen, other lymph nodes, adrenal glands, ovaries and testes, and possibly even the heart and brain. [186] These studies were of sub-optimal quality and will need to be repeated, but are very worrisome, if true. It is not normal, healthy, or wise for cells in these organs to be producing spike protein.

As already mentioned, we do not know how long the mRNA continues to make the cells synthesize the spike protein—only for a few hours, a few days, a few weeks, a few months, longer? Does this vary from person to person and from organ to organ? We also do not know how much spike protein is produced in a given person, or within various organs of a given person. This quantity might vary from person to person and within organs of an individual person. Some people and/or some organs may produce much larger quantities of spike protein than others. Nor do we know how much anti-spike antibody is produced by a given person and for how long. We also do not know the extent to which a given person’s immune system might mount a killer T-cell attack against the spike protein-coated cells, and for how long—this might vary from person to person and within organs of an individual person.

As just one example, if a particular young, vaccinated woman’s ovaries start making huge quantities of spike protein (compared to quantities produced by other vaccinated women) and her immune system mounts a particularly vigorous anti-spike protein antibody attack and/or a particularly vigorous and/or prolonged killer T-cell attack on spike protein-coated ovarian cells, that woman would be at risk of diminished fertility. This issue has not been adequately studied.

A fifth concern: Apparently a significant percentage of people are allergic to PEG. Some such people may have allergic reactions, including potential life-threatening anaphylaxis. How do we know who might have an initial or delayed allergic reaction to the PEG component of the vaccine?

A sixth concern: Are the mRNA vaccines setting people up for either transient or chronic autoimmune reactions? An example of this concern might be the Florida obstetrician who died of autoimmune thrombocytopenia shortly after receiving a mRNA vaccine. [187] Shoenfeld et al have emphasized the capacity of the SARS-CoV-2 virus to trigger a variety of autoimmune reactions, including reactions occurring due to “molecular mimicry.” [188-190] “A massive heptapeptide sharing exists between the SARS-CoV-2 spike glycoprotein and human proteins.” [188] There is a legitimate concern that the antibodies to spike protein that the mRNA vaccines train the immune system to produce might accidentally cross-react with peptides within normal human tissue (the phenomenon of molecular mimicry), either transiently, recurrently, or chronically. Although future studies might prove that the mRNA vaccines do not trigger significant molecular mimicry reactions, or other autoimmune reactions, this issue has not yet been adequately studied.

A seventh concern is the possibility that antibody dependent enhancement (ADE), or other similarly violent immune reactions, might occur in vaccinated people when, at a later date (many months, even years, later), they become infected with the wild SARS-CoV-2 virus. This has already been discussed under Question 8.

An eighth concern is that the spike protein all by itself can do great harm. [186, 191-208] This is true when the spike protein is present during active COVID illness, or when the spike protein is produced solely as a result of vaccination. Spike protein is a toxic, pathogenic (harmful) material. It can cause damage not only in people with active COVID illness, but also in vaccinated individuals (i.e., in the absence of infection). The spike protein can abnormally activate platelets, which predisposes to thrombosis (clotting). [192-194] The spike protein can also injure the endothelial cells that line the inner walls of blood vessels, which predisposes to thrombotic occlusion and/or conceivable microvascular occlusion from endothelial cell swelling. [195, 196, 200] The spike protein can cross the blood-brain barrier and potentially injure the brain. [197-199] The spike protein can lead to myocarditis, pericarditis, and lung injury. [17, 201, 202, 200]. And the spike protein can possibly injure the liver, causing immune-mediated hepatitis. [203-205] Again, this can occur due to vaccination alone, in the absence of ever being infected with the SARS-CoV-2 virus.

On the other hand, other published studies state that the COVID vaccines are quite safe. [209]

Unfortunately, the CDC/NIH has not been adequately documenting and studying adverse reactions to the COVID vaccines. One would think that part of the massive vaccination campaign, in which a potentially dangerous inadequately tested experimental vaccine is being given to billions of people, would include a compulsive, thorough, efficient, and mandatory monitoring system to document the extent and nature of adverse reactions. But no such system has been implemented. Only a voluntary, very cumbersome, inefficient system has been used—the Vaccine Adverse Events Reporting System (VAERS). This system captures only a minority of adverse events. [210]

Even with its gross inadequacies, the VAERS has reported a disturbing number of worrisome complications and deaths. [210-212] As of this writing, at least 7218 deaths have been reported in recently vaccinated individuals, in the USA. [210]. More deaths have been associated with the COVID vaccines in 8 months, than reported for all other vaccines (combined) over the past 17 years. Severe adverse events have included life-threatening blood clots, thrombocytopenia, myocarditis/pericarditis, branch retinal artery occlusion (BRAO), Bell’s palsy, Guillain-Barre, and other neurologic injuries. According to an epidemiological report from Public Health Ontario, since February 2021 there have been 106 incidents of post-vaccine myocarditis/pericarditis in people under age 25 in Ontario—31 of those cases in 12–17-year-old children. [213]

Despite the above VAERS data, the COVID Task Force and the mainstream media have barely mentioned these adverse events (other than “very rare” clots and “very rare” myocarditis) and have continued to confidently reassure the public that the vaccines are “safe.” Adverse reactions have been largely dismissed because they are “very rare” and “the benefits of the vaccine greatly outweigh the risks.” But are these statements true?

If the SARS-CoV-2 virus were as deadly as was initially feared (as deadly as SARS-1 or MERS), then the risks of vaccination, even if considerable, might be worth taking. But given the fact that the infection fatality rate of COVID is currently comparable to that of recent influenza viruses of above average severity; given the fact that healthy individuals under 60 (particularly children) are at very low risk of dying or being severely harmed by COVID; given the fact that excellent treatments are available for COVID (particularly for those who head into severe illness); given the genius and experience of the human immune system; given the worrisome potential and actual side effects of the vaccines and their role in possibly creating new worrisome variants of concern; given the mounting evidence of vaccine failure (see Question 11), and given all the other unknowns; the risks of the vaccine appear to outweigh the modest (at best) benefits—absolutely so for children. Out of an abundance of caution, it would seem wise to halt the vaccination campaign until adequate study of safety (and efficacy) has been done.

Who is correct? Are these COVID vaccines “quite safe,” or “quite dangerous?” Are they causing greater good than harm, or more harm than good?

As with Questions 7, 8, and 9, it would be wise to assemble an expert panel of fairly selected, internationally respected virologists and vaccinologists to carefully, critically, respectfully, and publicly examine this issue. As part of informed consent, the public certainly deserves to know and needs to know the full spectrum of side effects of these vaccines and the likelihood of their occurrence.

 

11. How effective were the COVID vaccines in the beginning? How effective are they now? Were they ever impressively effective?

When the COVID vaccines were first given Emergency Use Authorization (EUA) they were celebrated as being spectacularly effective—exceeding expectations and representing a monumental achievement of medical science. They were said to be in the range of “95% effective.”[214] The public was given the impression that if you got vaccinated and subsequently got exposed to the virus, you had a 95% chance of either not getting infected or experiencing only mild infection. The vaccines were said to at least protect against severe infection. [214] The further impression was that, of course, a small percentage of vaccinated people (5%) would be expected to get COVID, “because the vaccine is only 95% effective, not 100% effective.”

But on what basis were these claims made? Let’s look at the clinical trial conducted by Pfizer: [214]

In the Pfizer trial 21,720 people received the vaccine and 21,728 people received placebo. [214] The trial primarily consisted of documenting how many in each group subsequently developed a positive COVID PCR test during the trial period, which lasted only 2-3 months. Elderly people, pregnant women, and children were excluded from the study.

Of the 43,448 people in the study, 170 became COVID PCR positive (0.4%)—162 in the placebo group (0.74%) and 8 in the vaccinated group (0.036%). Importantly, the Ct values at which the PCR tests were positive were not discussed (meaning that we do not know how many of the positive results in each group were false positives); nor is it clear how many people in each group had well-documented evidence of absence of prior infection with COVID (meaning absence of both B and T cell immunity to COVID); nor is it clear that crowded working conditions and other exposure risks were equal in the two groups.

Ninety five percent (95%) of the people who became PCR positive (162/170) were in the placebo group and only 5% (8/170) of the PCR positive people (whatever that actually means) were from the vaccinated group. That, however, does not mean that 95% of vaccinated people will be protected from COVID by the vaccine. The only conclusion that can be drawn from these data is that of the 0.4% of people who became PCR positive (at who knows what Ct values), fewer were in the vaccine group than the placebo group (0.036% vs 0.74%)—i.e., there was a 95% “relative risk reduction” for development of PCR positivity (again, whatever that positivity means).

The “percent relative risk reduction” (even if none of the positive the PCR tests were false positives) does not, however, equal “true (real world) vaccine effectiveness” (the percent of people who will be protected from becoming infected when exposed to an infection-causing viral load). “Relative risk reduction” and “true (real world) vaccine effectiveness” are two very different things. They are not synonymous and should not be used interchangeably. A 95% “relative risk reduction” does not equal 95% “vaccine effectiveness.”

In order to claim that the Pfizer vaccine is 95% protective against COVID (a true vaccine effectiveness of 95%), it would be necessary to expose a large group of vaccinated subjects and a large group of unvaccinated subjects (both groups being equal in terms of average age, gender, extent of co-morbidities, and none with B or T cell evidence of prior COVID infection, etc.) to an equal (and considerable) viral load and then determine how many in each group developed a positive PCR test (at a Ct value less than 30), how many developed a positive genome sequencing test (which is far more accurate than PCR), how many became symptomatic (and to what degree), how many required hospitalization, how many required ICU admission, and how many died. If 1000 subjects were in each group and only 50 of the vaccinated subjects developed any of the above-mentioned evidence of COVID infection, then the data would suggest that the vaccine was 95% effective—because only 5% of exposed vaccinated subjects developed evidence of COVID. If 950 of the unvaccinated subjects developed evidence of COVID, that fact would provide additional evidence that the vaccine was protective, particularly if most of those 950 had at least moderate-severe disease (and if the 5% of vaccinated subjects who developed COVID had only mild disease). But, if only 5% of the unvaccinated group developed evidence of COVID, then one could not conclude that the vaccine was any more effective than placebo, particularly if the severity of illness in both groups was equal. One could conclude only that either the viral load used in the experiment was not sufficiently large to cause much illness in either group (meaning that the experiment would need to be repeated with a higher viral load); or the vaccine was no more effective than placebo.

Of course, the above experiment should not be done on human beings. However, a version of it could be done on animal subjects (PETA permitting), and if such a study showed that only 5% of the vaccinated animals developed COVID and it was mild in all cases, with no deaths; while 95% of unvaccinated animals developed COVID and it was moderate-severe in all cases, with 30% dying; then it could be concluded that the vaccine was approximately 95% protective in these animals.

But no such animal studies have been conducted with the COVID-19 vaccines.

Furthermore, when one analyses the Pfizer data in absolute terms: 0.74% (a very small percentage) of the placebo group developed a positive PCR test, while only 0.036% of the vaccinated group developed a positive PCR test. That is, less than 1% in either group developed a positive PCR test; and the vaccine reduced the incidence of PCR positivity (whatever that means) from 0.74% to 0.036%. This represents the “Absolute Risk Reduction” and does not represent a very impressive degree of efficacy (in this case an absolute risk reduction of less than 1%). Furthermore, without knowing the Ct values at which the PCR tests were positive, it is impossible to interpret the true significance of the difference in PCR results.

So, the claims of “95% efficacy” of these COVID vaccines are quite misleading, to say the least. Since no subjects in the Pfizer study died, it cannot be stated that the Pfizer vaccine prevents deaths. Although there were more instances of “severe illness” in the placebo group, more details and further/longer study are needed to determine whether these vaccines truly reduce the level of COVID disease severity. The data produced by these vaccine trials simply do not permit conclusions regarding how effective or ineffective these vaccines are in preventing or minimizing illness. Pfizer and Dr. Fauci have correctly admitted that these vaccines do not prevent virus from entering cells of vaccinated people, replicating there, and spreading to others—i.e., the vaccines do not prevent infection or transmission.

Not only is the short-term effectiveness of the vaccines unclear, the long-term effectiveness of the COVID vaccines is in doubt, especially with the newer variants. [215-221]. There is mounting evidence that the effectiveness of these vaccines wanes over the course of 3-6 months. [216-218] Natural immunity appears to be more robust and more durable than vaccine-induced immunity. [222-224]

When one looks at the longer-term real-world experience with these vaccines, the vaccines appear to be failing. The most instructive experience has been in Israel, which was the first country to roll out a rapid and massive vaccination campaign (using the Pfizer vaccine) and among the first to achieve a high percentage of vaccination of its citizenry (approximately 80%). In recent months, the predominant variant in Israel has been the Delta variant. The following has been observed in Israel:

After the initial roll-out of vaccination in Israel there was actually a quick rise (3-fold increase) in COVID cases, which peaked after 7-8 days and plateaued for the next 21 days—as if the vaccine were somehow causing a clinically significant degree of immunosuppression. Then, after day 28 (7 days after the second jab) there appeared to be some protection, which appeared to last 3-6 months and now seems to be waning. [225]

In March 2021 Israeli Ministry of Health data revealed 1566 deaths among 368,826 unvaccinated people (a death rate of 0.4%), while there were 898 deaths among 67,761 vaccinated people (a death rate of 1.3%). [226]

The Israeli Ministry of Health recently reported that during the week of July 11-17 there were 2996 confirmed cases of COVID in Israel. 84% of these cases occurred in vaccinated individuals. Unvaccinated people accounted for only 16%. [226, 227] During June and July 2021, COVID hospitalizations increased faster in the vaccinated than in the unvaccinated. Furthermore, vaccinated patients who are now developing COVID are dying at a greater rate than are unvaccinated Israelis who develop COVID. If this is true, one wonders if this is due, at least in part, to ADE phenomena occurring in the vaccinated when they become exposed to the SARS-CoV-2 virus, such as the Delta variant.

A recent Israeli study revealed that SARS-CoV-2 naïve vaccinees (i.e., vaccinees with no prior evidence of natural SARS-CoV-2 infection) were 13.04 times more likely to develop “breakthrough” infection with the Delta variant, compared to those who had previously been infected and were unvaccinated. [222]

In Israel, vaccination (not lack of vaccination) appears to be driving the development of new “variants of concern,” including the delta variant. [225]

More study is needed to confirm, reject, or refine the above observations. But the preliminary impression is that, in Israel, the rapid vaccination campaign is failing: Vaccination does not appear to be decreasing infection rates, severity of illness, or incidence of death, and it appears to be driving development of new variants of concern. The vaccination campaign appears to be causing more harm than good. In Israel, natural immunity appears to be far superior to vaccine-induced immunity.

A similar experience is occurring in the UK. Data published in a Public Health England briefing on September 3, 2021, reveal that since February 2021 70% of COVID deaths have occurred in vaccinated individuals. [26] Since February 2021 the death rate among unvaccinated individuals has been 0.2% while the death rate among all vaccinated (partial or full) individuals has been 0.5% and the death rate among fully vaccinated individuals has been 0.96%. By August 2021, the Delta variant was accounting for 99% of sequenced cases of SARS-CoV-2. The vaccines seem to be failing in the UK.

Data from the USA have been conflicting and difficult to interpret, primarily because of the extremely low quality of much US data. One recent report by the CDC reveals that during the month of July 2021, an outbreak of 469 cases of COVID occurred in Barnstable County, Massachusetts. 74% of these 469 cases occurred in fully vaccinated individuals. [228]

In a recent study in Viet Nam, fully vaccinated hospital workers became infected with the delta variant. [229] Nasal swabs from these workers revealed a viral load that was 251 times greater than the viral loads that had typically been seen in COVID cases during the pre-vaccine era. This suggests that the vaccination not only failed to prevent infection but actually enhanced viral replication within the vaccinated, converting them into super-spreaders. Those workers were, indeed, shown to infect patients and unvaccinated co-workers.

The vaccines, whose efficacy was not convincing in the first place, now appear to be failing greatly; they appear to be contributing to the development and spread of more worrisome variants; and they may be predisposing vaccinees to dangerous hyperimmune reactions (ADE) when they do become infected in the future.

To fully examine the extent to which the above worrisome impressions are true, it would be wise to assemble an expert panel of fairly selected, internationally respected virologists and vaccinologists to carefully, critically, respectfully, and publicly examine this issue. As part of informed consent, the public certainly deserves to know and needs to know the extent to which the COVID vaccines are effective and benefitting Humanity.

 

12. How urgent has been the necessity for vaccination?

So far, we have discussed the safety and efficacy of the COVID vaccines. How necessary have the vaccines truly been, and how much urgency has there truly been to provide vaccines?

According to the prevailing narrative (that espoused by the White House COVID Task Force and the CDC), there has always been great, urgent, desperate need for vaccination. This need and urgency was predicated, however, on data of very poor scientific quality that was generated by misuse of the COVID PCR test and poorly designed criteria for designation and documentation of “COVID cases,” “COVID hospitalizations,” and ‘COVID deaths.”

The sense of urgency was furthered by a failure to recognize the availability, efficacy, and importance of inpatient treatments for severe COVID illness and outpatient treatments of early mild COVID.

If proper scientifically sound data collection had occurred, and if the above treatments had been used, there probably would have been much less justification for the rushed, inadequately tested vaccination campaign that has been implemented.

According to the counter-narrative: vaccination has proven to be inadequately safe, inadequately effective, unconvincingly necessary, and unconvincingly urgent; the vaccination campaign has created more harm than good; and we would be far better off today, if this pandemic had not been managed with vaccination.

Which narrative is correct? As with Questions 7-11, it would be wise to assemble an expert panel of fairly selected, internationally respected virologists and vaccinologists to carefully, critically, respectfully, and publicly examine this issue. As part of informed consent, the public certainly deserves to know and needs to know the extent to which the COVID vaccines have been urgently needed.

 

13. What is likely to happen during the last few months of 2021? Will we see a worrisome surge of COVID?

The prevailing narrative: According to the prevailing narrative, a deadly surge of COVID will occur, because of the unwillingness of the unvaccinated to get vaccinated. This surge will result in children being hospitalized and dying in far greater numbers than has occurred during the first 18 months of the pandemic. All COVID deaths and hospitalizations will be the fault of the unvaccinated. This late 2021 surge could be prevented, if the unvaccinated would agree to be vaccinated. Hence the coercion, even requirement, for all, even children, to urgently become vaccinated.

The counter-narrative: There are some areas of disagreement within the counter-narrative group (Yeadon vs. Vanden Bossche, e.g.). But, overall, there is considerable concern (particularly if Dr. Vanden Bossche is correct) that, if the current vaccination campaign is continued, there will likely be a surge of COVID-related disease, hospitalizations, and deaths during the last few months of 2021, and it will be due to several factors:

1. 1. 1. The colder weather, the apparent increased transmissibility of the Delta variant (and possibly other emerging variants), and the worsening failure of the current vaccines to protect against these variants, will result in an increased number of people getting COVID—both vaccinated and unvaccinated people.
      2. Because vaccinated people may serve as producers, incubators, and relative super-spreaders for the new variants, they will infect unvaccinated people at a greater rate than in the pre-vaccine era, resulting in a further increase in the numbers of unvaccinated people (as well as vaccinated people) developing COVID.
      3. Some vaccinated people who become ill with COVID may become more ill than usual, because of ADE phenomena, including vaccinated children, and this would increase hospitalizations, ICU admissions, and deaths, particularly if helpful treatments continue to be under-utilized.
      4. If a more lethal variant emerges (thanks to the vaccination campaign), hospitalizations and deaths would further increase (among vaccinated and unvaccinated, including children).
      5. Hospitalizations may also increase because an increasing number of vaccinated people, including vaccinated children, may develop serious adverse reactions to the spike protein-producing vaccines and will need care for these complications of the vaccines (e.g., myocarditis, thrombosis, Guillain-Barre, etc.)
      6. All of the above would worsen if the current vaccination campaign is continued, particularly if it is expanded and accelerated.
      7. In other words, there is legitimate concern that the vaccination campaign has created an enormous mess; its continuation will create an even greater mess; and the greater mess will affect children. We would not be in this mess, if the pandemic had been handled without use of the currently available COVID vaccines.
      8. This mess will be even worse if the people in charge of the pandemic continue to discourage available inpatient and outpatient treatments for COVID, or if life-saving medications become scarce.

As with Questions 7-12, it would be wise to assemble an independent expert panel of fairly selected, internationally respected virologists, vaccinologists, and epidemiologists to carefully, critically, respectfully, and publicly examine this question. The public certainly deserves to know and needs to know what to expect and why. The public does not deserve to be held in suspense while chaos, doubt, fear, contradictory messaging, mystery, polarization, demonization, shaming, censorship, lack of dialogue, and lack of proper problem-solving reign.

 

14. Since many of the feared side effects of the vaccine (e.g., abnormal clotting and myocarditis, due to reactions associated with the spike protein) are quite rare, and since abnormal clotting and myocarditis (also associated with the spike protein) are common in severe COVID infection, wouldn’t it be wiser to get vaccinated in order to protect against abnormal clotting, myocarditis, and other harmful complications of COVID? Don’t the risks associated with infection outweigh the risks associated with the vaccine?

On the surface, the above questions would seem to represent a good argument for vaccination. However, there are problems with this way of thinking:

First, although abnormal clotting and myocarditis are common in people with severe COVID illness (particularly in patients who are not treated with prompt, appropriately aggressive interventions), these complications are not common in the vast majority of people who become infected with SARS-CoV-2. The vast majority of people who become infected with SARS-CoV-2 are either asymptomatic or have symptoms that do not require hospitalization, and this is particularly true of people under age 60, especially those under age 40.

Second, in both the vaccination setting and the setting of COVID infection, it is the spike protein that plays a major role in causing injury to tissues, including abnormal clotting and myocarditis. It needs to be understood that with natural COVID infection the spike protein is usually only briefly present, is present in relatively low quantity, and is present primarily in the respiratory tract—all thanks to our immune system’s ability to quickly neutralize the spike protein, kill the virus, and prevent its spread throughout the body. But with the vaccine the spike protein may be produced in much larger quantity; we do not know whether it is produced only for a few weeks, a few months, or even longer; and it may well be produced in many cells/organs throughout the body. So, exposure to the spike protein during natural COVID illness is not the same as exposure after vaccination. Furthermore, with vaccination you are guaranteeing exposure to the spike protein.

Third, the frequency with which worrisome side effects of the vaccine occur has probably been underestimated and under-reported. In young people, for example, vaccine-induced myocarditis is probably more likely to occur than is COVID-induced myocarditis. We do not know if this is true, because this issue has not, yet, been adequately studied. In other words, it is quite possible that among college and NBA basketball players, the likelihood of developing myocarditis from the vaccine is greater than the likelihood of developing myocarditis from natural COVID infection—particularly when considering that mass vaccination of all players guarantees that all of them will be exposed to the spike protein, whereas far less than 100% of players would be expected to develop worrisome COVID if unvaccinated.

Fourth, it is not so simple that the vaccine will protect a person from worrisome infection. As explained in the discussion of Question 11, the vaccines are probably much less effective than claimed, particularly now that new variants are “escaping” vaccine-induced antibodies.

So, for the above reasons (as well as many other concerns about the safety of the vaccines), it is not so simple that vaccination is wiser than remaining unvaccinated. At the very least, much more study of this issue is needed.

 

15. When health care systems, governmental agencies, and other organizations contemplate implementation of a mandatory vaccination policy, what should they consider before doing so? What are their obligations to the employee for whom they are mandating vaccination?

Mandating institutions and organizations have an obligation to provide complete information about the risks/benefits of the vaccine, and they must obtain informed consent from those who will be vaccinated. That process of informed consent must include thorough discussion of all side effect concerns and discussion of risks vs benefits. In order to provide full, honest information, the mandators must be fully informed themselves. They must be well-versed, regarding all of the questions discussed in this article. It is not okay to simply and confidently say, “These vaccines are safe, effective, and urgently needed.” Because these vaccines have not been sufficiently studied, such simplistic and confident statements are unwarranted and misleading.

The mandators must understand and share with the potential vaccinee that the currently available COVID vaccines have never been proven to be as effective as their manufacturers have claimed, and these vaccines appear to be rapidly losing whatever effectiveness they may have had as new variants develop and as time passes. (See Question 11, including the references provided in that discussion.)

The mandators must understand natural immunity and share that understanding with the potential vaccinee. There is growing evidence that people who have been infected with SARS-CoV-2 in the past (whether asymptomatic or symptomatic) and, thereby, have natural immunity to SARS-CoV-2, are not a risk to others, do not need to be vaccinated, and are at greater risk of developing vaccine complications, compared to those who have not had prior natural infection. Therefore, clinically, scientifically, and ethically, it is incumbent upon organizations who are vaccinating employees to determine, first, the status of an employee’s natural immunity against the SARS-CoV-2 virus, either by history of COVID illness or by lab testing—and lab evaluation should include not just with antibody testing, but also testing of the employee’s T-cell immunity against SARS-CoV-2.

It is unethical for an organization to vaccinate an employee without first determining the employee’s status regarding prior SARS-CoV-2 infection and natural immunity to the virus. This must be done even for employees who are eagerly seeking vaccination. At the very least, all people who are about to be vaccinated need to be fully informed of the need for this just-mentioned assessment/testing. To proceed without discussion of that need represents failure to comply with rules of informed consent.

The mandators must be aware of, and share, the following concern: There is growing evidence that the vaccination campaign (not unvaccinated people) is responsible for producing worrisome new variants. and there is growing evidence that vaccinated people may become “super-spreaders” that pose a threat to fellow workers and to the potential vaccinee’s own children. (See Questions 7, 9, 11, and 13 and reference 229 in particular, Chau et al.)

In other words, vaccinated health care workers may soon (or already) be a greater threat to patients than unvaccinated workers. In fact, unvaccinated workers who have had prior SARS-CoV-2 infection are the safest workers for the health care sector—meaning that they are not a threat to others and are not at risk themselves. They have robust, durable immunity and are more likely to successfully handle new variants than are vaccinated individuals.

In short, the mandators must know about all of the concerns discussed in Questions 7, 8, 9, 10, 11, 13, and 14 and must thoroughly discuss these concerns with employees before they are vaccinated. Otherwise, the employees will be vaccinated in the absence of proper informed consent. Such failure to properly obtain informed consent is unethical and illegal—i.e., criminal.

All of the above concerns and facts must be taken into account when organizations consider mandating vaccination of their employees. Included in this consideration is whether the organization is willing to assume full liability for any adverse effects suffered by a person who is coerced into taking a mandated vaccine, and whether the organization is willing to fully and fairly compensate employees whose employment has been wrongly terminated because of their unwillingness to participate in a vaccination campaign that is dangerous for them and for others.

Given what is known and unknown about COVID issues, it is profoundly inappropriate for government, health care, and business organizations to fire employees for declining COVID vaccination or to raise their health insurance premiums.

Before mandating COVID vaccination, public and private organizations must consider the above scientific, medical, ethical, moral, financial, and legal obligations they must honor.

 

16. What percentage of people at a large gathering (e.g., at a high school basketball game) might be infected with SARS-CoV-2 and might transmit the infection to others? Are 15%, 10%, 5%, 2%, 1% of such people infected? How risky is it to attend such an event?

The best available data on this issue have been provided by the National Health Service (NHS) in the United Kingdom (UK), where a series of randomized representative community prevalence surveys have been conducted on a roughly monthly basis since May 2020. [230] With each survey a random nationally representative sample of individuals were tested (using a COVID PCR test) to determine, on a particular given day, the percentage of the population who might have COVID and might, thereby, potentially transmit the virus to others.

In the most representative set of the NHS/UK surveys (surveys 2-7) 979,709 individuals were tested. 88.9% of these individuals reported no symptoms during the week prior to testing. [230] 11.1% had one or more of 26 potential symptoms that would be compatible with COVID. Of the 88.9% who were asymptomatic, 0.3% had a positive COVID PCR test (1 out of every 333 people). Of the 11.1% with at least one symptom, 1.4% were PCR positive. Of the entire group of 979,709 individuals, 0.46% were PCR positive—i.e., 1 out of every 217 people.

The above percentages represent mean values for aggregate data from the 6 surveys. The percentages for each individual survey were, unfortunately, not readily apparent and probably varied, depending on the season of the year and whether a surge of COVID was occurring at the time of the survey.

The above data suggest that if all people attending a high school basketball game were tested (via PCR) upon entry to the gymnasium, 0.46% (1 in 217) could be expected to be PCR positive—0.3% if only asymptomatic individuals were permitted to enter the gymnasium.

However, it must be realized that the above data cannot be adequately interpreted without knowing the Ct values of all the positive PCR tests. (Please see Articles #3 and #15 on the website, with their references.) If a person’s PCR test is positive at a Ct value of 30 or less, then it is likely that that person had truly become infected with SARS-CoV-2 infection and might be infectious (contagious, a threat to others). [89-112] The lower the Ct value at which the test is positive, the more likely it is that the person has truly been infected and the more likely it is that they are infectious. If a person’s PCR test is positive only at a Ct value of 35 or higher, there is a very good chance that their result represents a false positive, and even if their result represents a true positive, it is extremely unlikely that such a person is infectious at that time. In either case, those people with a positive PCR at a Ct of 35 or higher are not contagious and do not represent a threat to others. [110-112]

Unfortunately, the NHS/UK data (surveys 2-7) do not include a breakdown of how many of the positive PCR tests were positive at a Ct of 30 or lower and how many were positive at a Ct of 35 or higher. These missing data are extremely important, particularly when trying to interpret a positive PCR result in a person who is asymptomatic and has been randomly selected to participate in a screening survey (like surveys 2-7). Other studies have suggested that approximately 90% of positive PCR tests occurring in surveillance screening surveys (like surveys 2-7) are positive at Ct values greater than 30, which means that the vast majority (possibly close to 90%) of the asymptomatic individuals (in surveys 2-7) who had a positive PCR test were not infectious and many of them probably had false positive tests. [231, 232]

Based on the above, if only asymptomatic individuals were allowed into the high school gymnasium, then 0.3% would be expected to be PCR positive, but as many as 90% of these positive individuals would not be expected to be contagious/infectious (because their test is positive at a very high Ct value and, therefore, is either a false positive or means they have been infected but are extremely unlikely to currently be contagious). If only 10% of the 0.3% are truly contagious, that means only 0.03% are contagious—which translates to 1 out of 3330 people being a possible threat.

To what extent, therefore, should a high school student be fearful of attending a high school basketball game, if possibly as few as 1 in 3330 people in the gymnasium is likely to represent an infectious threat—particularly when one considers that even if the student happens to contract infection in that gymnasium, the odds of him/her dying of COVID are 1 in 37,037 (even less than that, if treated optimally).

Much more study of the point prevalence of SARS-CoV-2 infection in various communities is greatly needed, and those studies should not be based on COVID PCR tests alone or on COVID antigen tests. Those studies should be based on genome sequencing of all positive PCR tests, and the viral load associated with each positive test must be determined (either by recording the Ct value at which each test was positive, or by performing a reliable quantitative test for viral load). In the meantime, the above discussion provides helpful perspective (at least tentatively), until data of higher quality and quantity are available.

So, the answer to Question 16 is that we are not yet sure, because available data have been of low quality and quantity. But best available data suggest that in a random sample of asymptomatic individuals the percentage of people who might be an infectious threat to others may be as low as 0.03% (not 15%, 10%, 5%, 2%, or 1%, but far less than even 0.3%).

 

17. What are the keys to successful resolution of the COVID pandemic?

My best guess is that the keys to successful resolution of the COVID pandemic will include:

1. 1. 1. Restoration of careful critical thinking, scientifically sound examination, and healthy dialogue—within the medical community and the public.
      2. Massive, honest, and accurate public education—with all citizens doing their homework to the best of their ability.
      3. Immediate establishment of panels of fairly selected and internationally respected scientists, scholars, and citizens—an “Independent International COVID Commission”—to examine and draw best possible conclusions about the questions raised in this article. These panels would model the needed critical thinking, scientifically sound examination, and healthy dialogue that the public would be encouraged to emulate, and their findings would serve as the major source for the public education about COVID. The dialogue of these panels would be televised globally and completely, so that the public could decide who seems most honest, knowledgeable, careful, and wise.
      4. Establishment of scientifically sound COVID data collection—for the first time (at least in the USA) since onset of this pandemic. This includes proper use of the PCR test and confirmation with Sanger sequencing. It also includes scientifically sound diagnostic and classification criteria.
      5. Reversal of polarization, demonization, extremism, intolerance, shaming, and censorship.
      6. Cessation of media creation of excessive fears.
      7. Shutdown of the mass vaccination campaign ASAP—out of an abundance of caution, until adequate safety studies have been done.
      8. Maximization of optimal outpatient and inpatient treatment for COVID, including assurance that needed medications will be in adequate supply.
      9. An open-minded willingness to challenge long-held preferred beliefs and to replace those that are lacking truth with more accurate understandings.
      10. A new appreciation of and respect for the astonishing genius and competence of the human immune system.
      11. Thorough investigation of the origin of SARS-CoV-2 (see below).

18. How did the SARS-CoV-2 virus come about in the first place? Did it occur naturally, by hopping from a bat to humans? Or was it bio-engineered and then leak from a laboratory?

For the sake of minimizing future pandemics and better understanding the current pandemic (including how to optimally treat individual patients), it is imperative that we determine why/how this pandemic got started. Regarding the origin of the SARS-CoV-2 virus, each of the following hypotheses needs to be carefully examined:

1. The virus developed naturally and spontaneously in the wild—i.e., a bat coronavirus happened to mutate in a way that permitted it to “hop” from bats to humans (“zoonotic jump”)—possibly with pangolins serving as an intermediary.
2. The virus developed unnaturally in the wild because of encroachment of human beings on the natural habitat of bats—an encroachment that facilitated zoonotic jump of a bat coronavirus virus from bats to humans.
3. The virus was bio-engineered (using a bat virus as the backbone) in a research laboratory as part of a well-meaning protective, defensive effort to counter biological warfare that could potentially be waged at some point by a nefarious adversary—and the virus either accidentally “leaked” out of the lab or was nefariously leaked by a deranged individual(s).
4. The virus was nefariously bio-engineered in a research bioweapons laboratory with an intention to eventually intentionally leak the virus.

The best way to begin investigation of the above hypotheses is to carefully examine the genomic structure of the virus. Most of what is explained below comes from a presentation by Michael Palmer, MD, a Canadian physician and biochemist. [233] His understanding is based largely on the work of Dr. Li Meng Yan.[234, 235] His conclusions are consistent with those of many eminent virologists, including Dr. Luc Montagnier, the French virologist who won the Nobel Prize for discovery of HIV. [236-239] For comparison, the report of the US House Foreign Affairs Committee Report on The Origin of the COVID-19: An Investigation of the Wuhan Institute of Virology can be reviewed. [240]

Before accepting Dr. Palmer’s explanations as fact, however, it would be wise to assemble an expert panel of fairly selected, internationally respected virologists and molecular biologists to carefully, critically, respectfully, transparently, and publicly examine this issue. The public certainly deserves to know and needs to know how the SARS-CoV-2 virus came into being.

Dr. Palmer’s explanation:

An initial important observation is that the spike protein of the SARS-CoV-2 virus binds more perfectly with the ACE-2 receptor of humans than with the ACE-2 receptor of bats. This is the opposite of what would be expected if this virus appeared via zoonotic jump. If the virus jumped from a bat, one would expect the spike protein to bind more perfectly with bat ACE-2 receptors than human ACE-2 receptors.

Li Meng Yan has proposed that the receptor binding domain (RBD) of the SARS-CoV-2 virus (the RBD is that part of the spike protein that actually binds to the ACE-2 receptor) was bioengineered, starting with the RBD of the SARS-CoV-1 virus and experimentally modifying it so that it would bind well to human ACE-2 receptors. In support of this hypothesis is the fact that the DNA sequence that encodes the RBD of SARS-CoV-2 is book-ended by two particularly revealing restriction sites—Eco R1 and BstE11. These two restriction sites are commonly used in laboratory recombinant DNA experiments and are very unlikely to appear naturally. These two restriction sites were clearly engineered into the SARS-CoV-2 virus, because the likelihood of these two sites appearing naturally would be 1 in 24 million. So, the fact that the RBD is book-ended by these two tell-tale restriction sites strongly suggests that SARS-CoV-2 was bioengineered in a laboratory.

Another feature of the virus that suggests a lab origin is the presence of a Furin cleavage site. A Furin cleavage site does not exist in SARS-CoV-1, nor does it exist in any other coronavirus. The presence of this site is very unusual. The best explanation is that it was bioengineered into the virus. Furin is a protease (an enzyme) that is located in all nucleated cells in the human body, which means most human cells. The Furin cleavage site enables the SARS-CoV-2 virus to more easily enter nucleated cells of the human body. This suggests that SARS-CoV-2 was bioengineered to be better able to enter a broad range of cells within the human body—i.e., infect a greater variety of organs, thereby making it a more problematic and potentially more lethal virus.

Furthermore, the genome of the SARS-CoV-2 virus contains mutations that enable recruitment of a second cellular receptor, called CLEC 4M. This further enables the SARS-CoV-2 virus to enter a broad range of human cells—i.e., to infect a greater variety of cells and organs.

All of the above mutations—the two restriction sites (EcoR1 and BstE11), the Furin cleavage site, and the CLEC 4M-related mutation—are very unlikely to have occurred naturally and have undoubtedly been bioengineered into the virus. It is statistically impossible that all of the unique features of the SARS-CoV-2 genome could have appeared naturally (i.e., via zoonotic jump). The genome shows clear evidence that the virus was manipulated via use of recombinant DNA technology. The RBD of a bat coronavirus (SARS-CoV-1) was removed, using recombinant DNA technology, and a new modified and optimized RBD was inserted (engineered in). And this was done to enable better infectivity of human cells and organs. This represents “gain of function” manipulation. The rest of the SARS-CoV-2 virus is very similar to ordinary bat viruses.

Most coronaviruses primarily infect respiratory cells and are unable to infect other cells to any clinically significant degree. The insertions of the optimized RBD, the Furin cleavage site, and the CLEC 4M mutations are important because they enable SARS-CoV-2 to more easily infect a wide variety of non-respiratory cells and organs, including the heart and the brain. This may explain some of the unusual and frightening clinical features of severe COVID.

According to Dr. Palmer, the natural “zoonotic jump” hypothesis simply does not fit.

Unfortunately, the research Yan and others have done to document the above evidence for a bioengineered virus has been censored and denied publication.

So, according to Dr. Palmer, the SARS-CoV-2 virus represents a deliberately bioengineered virus. This notion has received solid support from many eminent scientists, including Dr. Montagnier, the Nobel prize winning virologist who discovered HIV. Dr. Montagnier is convinced that the SARS-CoV-2 virus was bioengineered in a laboratory.

Dr. Palmer goes on to explain: Although SARS-CoV-2 was apparently deliberately bioengineered to be a particularly lethal virus, its bioengineers, fortunately, failed to make it as virulent as some might have hoped. The human immune system’s ability to counteract SARS-CoV-2 (via cross-reactive capabilities gained from past coronavirus experiences) has probably been much more effective than the bioengineers anticipated. The fact that the bioengineers failed to remove the tell-tale restriction sites suggests that the bioengineering process was rushed, resulting in needed improvements not being made. Fortunately, the final product, SARS-CoV-2, has turned out to be much less virulent than it could have been. Its virulence appears to be comparable to that of an above-average influenza virus. The previously mentioned insertions of Furin cleavage sites and CLEC 4M mutations have, however, probably contributed to the clinical observation that SARS-CoV-2 appears to have an unusual ability to infect a broad range of human cells, beyond the respiratory tract, including the heart and brain.

Dr. Palmer thinks it makes most sense that this virus was unleashed on purpose, rather than accidentally. If its release had been accidental, one would think that authorities would have tried to minimize the seriousness of the accident, or at least not maximized fears—i.e., downplay fears regarding consequences of the accident. Instead, fears about the virus were initially maximized and have continued to be maximized ever since.

Again, it would be wise to assemble an expert panel of fairly selected, internationally respected virologists and molecular biologists to carefully, critically, respectfully, and publicly examine this issue—to verify, modify, or reject the conclusions of Dr. Palmer, Dr. Yan, and Dr. Montagnier. The truth about this issue is extremely important.

 

19. If SARS is a bioengineered pathogen that has been deliberately released, why has this been done?

Why would anyone do such a horrible thing? Before speculating on that question, let’s ask a few additional questions. Why, since the beginning of the pandemic, have those in charge excessively stoked fears by misusing the PCR test to produce alarming case numbers and by using excessively broad definitions of COVID hospitalizations and COVID deaths to excessively frighten the public? Why would the people in charge discourage use of life-saving inpatient treatments and demonize use of safe outpatient treatments? Why would they largely ignore natural immunity and insist that the only solutions to the pandemic are vaccines and fluctuating degrees of lockdown? Why has only one COVID narrative been allowed? Why have the insights and concerns of eminent virologists, immunologists, molecular biologists, and caring physicians who have challenged the prevailing narrative been censored and punished—some of them losing their licenses for simply asking and discussing questions? Why has public education about COVID not included mention of Ct values, effective treatments, the suboptimal quality of COVID data collection, the worrisome side effects of the vaccines, and the unusual genomic characteristics of the virus itself? Why has critical thinking and healthy dialogue been discouraged and replaced by encouraged and uncorrected polarization and intolerance? Why have the safety, efficacy, necessity, and urgency of vaccination been overstated? Why have those who have carefully examined the pandemic and have warned against vaccination been demonized and ignored? Why have the unvaccinated been blamed for continuation of the pandemic and even called “murderers?” Given all the confusion surrounding COVID and given the huge differences of scientific opinion, why has the White House COVID Task Force, the NIH, and the CDC not called for establishment of an “Independent International COVID Commission” (consisting of fairly selected, internationally respected expert panels) to carefully, critically, respectfully, and publicly examine and resolve these issue?

It is difficult to fathom why anyone would do the above—especially create a dangerous virus, deliberately unleash it on the public, then cover up what has happened. But out of an abundance of caution, we need to at least consider and investigate this possibility. If this has occurred, it is important to imagine and determine why. Most likely, the reasons would have to do with a pathological desire for power, control, and wealth. Most likely, the people responsible, would be people who already have immense power, control, and wealth, are fearful of losing it, and are operating with enormous arrogance, ignorance, and hubris and very little empathy or compassion. Many of them might believe they have been doing the right thing. Others might simply be “following orders” and “going along to get along.”

If it is eventually proven that SARS-CoV-2 was bioengineered in the Wuhan Lab, then unleashed on the public, it is important to avoid jumping to the conclusion that China, alone, was responsible. The US NIH has at least indirectly funded “gain of function” viral research, and US, French, and Canadian scientists closely collaborated with the Wuhan Lab prior to the onset of the pandemic. A more likely hypothesis would be that a transnational consortium of collaborating ultra-wealthy, ultra-powerful, ultra-controlling individuals from several countries (USA, China, European countries, Canada, for example) were involved in the planning and funding of such an operation. (See Articles #19 and #20 on the website.)

Crimes against humanity have happened before. It is wrong, for example, to deny the Holocaust. The perpetrators of Nazi crimes needed to be stopped and held to account in Nuremberg. Likewise, if it is proven that this COVID pandemic has been due to a bioengineered virus that was unleashed on the public, it would be wrong to deny that crimes against humanity have been committed by the perpetrators of the pandemic. If such is proven to be true, those perpetrators must be stopped and held accountable.

As mentioned with several of the other questions, it would be wise and extremely important to assemble an expert panel of fairly selected and internationally respected individuals—an Independent International COVID Commission—to carefully, critically, respectfully, and publicly examine this issue.

 

20: If the prevailing COVID narrative has been inaccurate, why have so many people (30-70% of the US population?) embraced this narrative?

This question has been addressed in a helpful way by Professor Mattias Desmet, a clinical psychologist and psychoanalyst at the University of Ghent in Belgium. [241-242] Professor Desmet has explained the concept of “mass-formation” (“massenbildung”) and why this concept is relevant to the COVID situation. His explanation of mass-formation is paraphrased below:

Mass-formation is a group psychological phenomenon in which a majority of the public becomes willing to accept a narrative (and that narrative’s associated public policies), despite the possibility that the narrative may be inaccurate and its policies may be detrimental to Humanity. An increasing amount of Mass formation allows an increasing amount of totalitarianism to develop and become established.

The concept of mass-formation is based, in part, on the insights of Gustave Le Bon (a French sociologist and physician who published “The Crowd: A Study of the Popular Mind in 1895), Hanna Arendt (who published The Origins of Totalitarianism, in 1951), and some of Sigmund Freud’s insights on group psychology.

Desmet explains that there are four pre-conditions that predispose to development of mass formation and pave the way towards increasing totalitarianism:

• Lots of social isolation: A large percentage of people feel socially isolated. They experience a lack of social connection. We are social beings. We long for both small scale and large-scale social connection.
• Lack of a sense of meaningfulness: A large percentage of people sense a lack of meaningfulness in their lives. They long to be part of something more meaningful, something bigger than themselves. They long to be part of a noble, meaningful cause. They wish their lives had more purpose and meaning.
• Lots of painful free-floating anxiety (FFA) and fear: Lots of people are anxious, unsettled, and fearful, with much of their anxiety and fear being non-specific, un-tethered to any identifiable cause—free-floating anxiety and fear that have no particular focus and, therefore, no apparent solution. They long for a focal point—something specific to which they can attribute their anxiety, so that they can take specific action to reduce their anxiety, pain, and fearfulness.
• Lots of free-floating psychological discontent: A large percentage of the population senses that their personal lives and the social milieu they live in are lacking emotional health and spiritual depth. They sense too much social disorder and social dysfunction. They long for healthier and more stable social arrangements.

Once the above preconditions have developed and affect a large percentage of the population, people in positions of power can develop an attractive (but not necessarily accurate) narrative that provides a focal point for the free-floating anxiety—a narrative that provides something specific to which people can attach their untethered anxiety and provides a plan to deal with this focal point. The narrative provides a specific “object of anxiety,” a specific thing people can blame for their anxieties and collectively fight against.

Encouraged and informed by the narrative, people start to collectively and enthusiastically band together to defeat the “object of anxiety” provided and explained by the narrative. This offers a new social connectedness, new social bonding, new meaningfulness, new purpose, new “sense making,” an attractive and even exhilarating feeling of being part of something noble and bigger than oneself. Suddenly people’s attention is fully focused on collectively fighting a narrowly focused battle against the named enemy. People increasingly believe (mostly subconsciously) that the narrative and their participation in its directives will successfully assuage the angst-producing issues with which they have been struggling (the four preconditions mentioned above).

Unfortunately, this massive increase in social connectedness, which is narrowly focused and may be based on an inaccurate narrative, may lead to a form of unhealthy “mental intoxication.” Those who become most committed to the narrative and its policies may become aggressively intolerant of those who challenge the narrative—because they (believers in the narrative) do not want to return to a state of painful free-floating anxiety; they prefer to remain in their less painful state of mental intoxication. Those who challenge the narrative tend to be viewed as threatening “enemies of the people.” Believers in the prevailing narrative may direct aggression towards the dissidents, while becoming increasingly willing to accept controlling policies that they normally would not tolerate.

If the prevailing narrative is largely inaccurate and promotes anger and action against an undeserving and inaccurately determined “enemy,” the above process leads to increasing degrees of abusive intolerance, discrimination, and totalitarianism.

Mattias Desmet is concerned that the four preconditions mentioned above have long existed in Europe and North America and are now predisposing a large percentage of the public to accept (and inadequately question) an inaccurate COVID narrative that is narrowly focusing attention on the SARS-CoV-2 virus, is leading people to accept increasing degrees of totalitarianism, and is leading people to become increasingly intolerant themselves. He estimates that perhaps 30% of the European and North American populations have enthusiastically fully embraced this narrative; and an additional 40% have passively accepted it, despite having doubts and questions about it. He estimates that the remaining 30% of the population is comprised of a heterogeneous group that is unwilling to accept the narrative, for a variety of reasons and to varying degrees.

As with the other questions addressed in this article, it would be wise to assemble a panel of internationally respected psychologists, psychiatrists, sociologists, political philosophers, and historians who are experts in mass psychology and the history of Nazi Germany and Stalin’s Soviet Union, to discuss the extent to which mass-formation and totalitarianism are, or are not, developing during the COVID pandemic.

 

TENTATIVE CONCLUSIONS:

The following conclusions are tentative and are made in a spirit of exercising an abundance of caution—until the above 20 questions presented in this article are thoroughly, objectively, and respectfully addressed by proposed panels of fairly selected and internationally respected experts in the fields of virology, epidemiology, vaccinology, molecular biology, infectious disease, general medicine, intensive care, laboratory medicine, ethics, public health, public policy, psychology, sociology, history, economics, and geopolitics—sub-panels of an “Independent International COVID Commission.” Full investigation of, and healthy dialogue about, the 20 Questions discussed in this article is absolutely and desperately needed. The public deserves and needs honest answers.

In the meantime, the tentative conclusions below make the most sense to me:

• Though certainly capable of causing severe illness and death, the intrinsic virulence (deadliness) of the original SARS-CoV-2 virus was comparable to that of the 2017-18 seasonal influenza virus (which was an influenza virus of above-average severity).
• The subsequent variants of the SARS-CoV-2 virus, including the current Delta variant (probably), have not been more virulent than the original SARS-CoV-2 virus. There is legitimate concern, however, that the current mass vaccination campaign may drive the development of a more virulent variant in the future (as per Dr. Vanden Bossche). Out of an abundance of caution, this possibility needs to be taken seriously. It seems more likely, though, that Dr. Yeadon is correct—that more virulent strains will not appear.
• The Delta variant (and future variants) may be more transmissible, but the extent to which this is definitely true is unclear.
• Though SARS-CoV-2 has, so far, not been more virulent than the 2017-18 seasonal influenza virus, COVID does have several unusual and frightening clinical features (e.g., clotting, brain and heart involvement)—probably due to entry of the virus into a broader range of human cells/organs and circulation of the spike protein far beyond the respiratory tract.
• Since the beginning of the pandemic, excellent inpatient treatments have, fortunately, been available for severe COVID illness. Unfortunately, these treatments were initially officially discouraged and have been inadequately used throughout the course of the pandemic. This has likely led to many unnecessary hospitalizations and deaths.
• Since the beginning of the pandemic, appropriate outpatient treatments have been available for treatment of early COVID. These treatments have appeared to substantially reduce likelihood of progression of mild COVID to severe COVID. It has been estimated that these outpatient treatments could reduce hospitalizations and death by as much as 85% and 75%, respectively. Unfortunately, these treatments and their advocates were quickly, summarily, unscientifically, and unfairly demonized by those in charge of the pandemic. As a result, these treatments have been under-utilized (at least in the USA) throughout the pandemic. This has likely led to many unnecessary hospitalizations and deaths.
• Unfortunately, the COVID PCR test, which has served as the primary basis for diagnosis and epidemiological data collection, has been used in an incorrect, unscientific, and very misleading way. This has resulted in unreliable, misleading data, regarding COVID cases, hospitalizations, and deaths.
• Epidemiologic data collection has been further compromised by a failure to develop and implement strict and accurate criteria for designation of a COVID case, COVID hospitalization, and COVID death. As a result, we do not know how many true COVID deaths have occurred.
• The COVID mass vaccination campaign, which uses sub-optimal vaccines, appears to be driving the development of “escape” mutations, such as those of the Delta variant. These particular variants, which would not have been likely to appear in the absence of such vaccination, tend to become increasingly infectious (transmissible); enjoy enhanced replication within the vaccinated; are spread to others (particularly by the vaccinated); and have potential to eventually become more virulent (if Dr. Vanden Bossche is correct).
• The COVID vaccines have not been nearly as effective as they have been claimed to be. The repeated claim of “95% efficacy” is quite misleading. These vaccines are becoming more ineffective as the vaccination campaign continues.
• The COVID vaccines are not nearly as safe as they have been purported to be. In fact, they appear to be quite dangerous, causing unacceptable levels of death and injury. They have been very inadequately tested.
• The vaccines may predispose vaccinated people to develop ADE (antibody-dependent enhancement), a phenomenon that increases the vaccinated person’s likelihood of experiencing a life-threatening hyperimmune reaction to future SARS-CoV-2 infection. The frequency with which ADE will occur and the extent to which it will be severe are currently unclear and require careful prospective study.
• The current VAERS system is woefully inadequate for study of COVID vaccine-related side effects. A new, mandatory, scientifically rigorous, adequately funded, and adequately staffed VAERS system is desperately needed.
• In addition to properly documenting vaccine injuries, we need to immediately and thoroughly study how to best treat injuries caused by the COVID vaccines. This should include NIH/FDA funded large, nation-wide, randomized controlled trials of prompt immunosuppressive treatment of immune-mediated injuries caused by the vaccine—such as immune-mediated myocarditis/pericarditis and immune-mediated neurologic disease caused by the vaccine. Vaccine-injured people deserve such immediate study and care.
• The mass vaccination campaign has possibly caused prolongation of the COVID pandemic and made it more threatening to all, including children.
• At its current stage, the pandemic is not a “pandemic of the unvaccinated.” Instead, it is a pandemic that has possibly been made worse by the vaccination campaign.
• We would be much better off at this point if the response to the COVID pandemic had never included deployment of the current COVID vaccines. It would have been better to rely on natural immunity, prompt and appropriately aggressive outpatient and inpatient treatment, and common-sense public health practices.
• There was never urgent need to implement a mass vaccination campaign, particularly with such inadequately tested vaccines, particularly when successful non-vaccine treatments have been available.
• The natural immunity developed after infection with SARS-CoV-2 is far superior to vaccine-induced immunity. Natural immunity to SARS-CoV-2 is more competent, protective, safe, and durable than the immunity induced by currently available COVID vaccines. People who have already experienced COVID do not need COVID vaccination. In fact, it is dangerous to vaccinate people who have already developed natural immunity to SARS-CoV-2 through natural infection.
• Because people with natural immunity to SARS-CoV-2 need not and should not receive COVID vaccination, it is imperative to develop tests for documentation of natural immunity to SARS-CoV-2. Those tests should reliably test for both B-cell and T-cell immunity against SARS-CoV-2. Those tests should be made readily available (free of charge), they should be used, and they should be honored.
• Instead of mandating that people with prior COVID be vaccinated, it should be realized that unvaccinated people with evidence of natural immunity against SARS-CoV-2 are the very best people to be working in hospitals, clinics, nursing homes, and other places of employment—because they will not become infected, and they will not spread infection. They are not a threat to others and others are no threat to them.
• For most people, particularly the young, any benefits of the currently available COVID vaccines are substantially outweighed by the risks.
• Those who have declined vaccination have been on the right side of science, medicine, ethics, the law, democracy, and history.
• If the current vaccination campaign is continued, and particularly if Dr. Vanden Bossche is correct, there is risk that a surge of COVID-related disease, hospitalizations, and deaths will occur during the last months of 2021, and this will likely be due to several factors:
  • The colder weather, the apparent increased transmissibility of the Delta variant (and possibly other emerging variants), and the worsening failure of the current vaccines to protect against these variants, may result in an increased number of people getting COVID—both vaccinated and unvaccinated people.
  • Because vaccinated people may serve as producers, incubators, and relative super-spreaders for the new variants, they will infect unvaccinated people, resulting in a further increase in the numbers of unvaccinated people (as well as vaccinated people) developing COVID.
  • Some vaccinated people who become ill with COVID (due to breakthrough infection) may become more ill than usual, because of ADE phenomena, including vaccinated children, and this would increase hospitalizations, ICU admissions, and deaths, particularly if helpful treatments continue to be under-utilized.
  • If a more lethal variant emerges (thanks to the vaccination campaign), hospitalizations and deaths would further increase (among vaccinated and unvaccinated, including children).
  • Hospitalizations may also increase because an increasing number of vaccinated people, including vaccinated children, may develop serious adverse reactions to the spike protein-producing vaccines and will need care for these complications of the vaccines (e.g., myocarditis, Guillain-Barre, etc.)
  • All of the above would worsen if the current vaccination campaign is continued, particularly if it is expanded and accelerated.
  • In other words, there is legitimate concern that the vaccination campaign has created an enormous mess; its continuation will create an even greater mess; and the greater mess will affect children.
  • This mess will be even worse if the people in charge of the pandemic continue to discourage available inpatient and outpatient treatments for COVID, or if life-saving medications become scarce.
  • This mess will further worsen if adverse side effects of the vaccine are ignored, under-studied, and under-treated.
• Given the above concerns, the COVID vaccination campaign should, out of an abundance of caution and until more is known, be immediately shut down, world-wide. It does not appear to be safe, effective, necessary, or wise, and it may be making matters worse.
• Mandatory vaccination should be outlawed immediately.
• Within the medical/scientific community there have been enormous and unresolved differences of opinion, regarding the questions/issues raised in this article. This has led to enormous and growing levels of confusion, fear, anxiety, cognitive dissonance, polarization, mystification, division, extremism, intolerance, anger, shaming, name-calling, censoring, and impatience within the public—including political and corporate leaders, the media, and the medical community itself.
• The above consequences of unresolved and festering confusion, fear, and anxiety have been greatly traumatizing to Humanity, particularly to children. Fear and anxiety, by themselves, may be interfering with people’s ability to think clearly, thoughtfully, and carefully.
• There is need to determine the extent to which “mass-formation” and totalitarianism have evolved during this COVID pandemic.
• Given the above consequences of unresolved confusion and increasing division, it is perplexing why the leaders of the national and international response to COVID (the White House COVID Task force, CDC, NIH, WHO) have not (long ago) called for the establishment of an “Independent International COVID Commission” to help resolve conflicts and clarify what is most likely true and what is less likely to be true—a Commission consisting of multiple panels of fairly selected, internationally respected experts in their fields. Such is the tradition of science, medicine, democracy, and civil society.
• It has been abusive to keep the public, particularly children, in a perpetual state of unresolved confusion, fear, anxiety, mystification, and insecurity. This abusive situation was preventable. It should have been prevented long ago (at least 18 months ago).
• Keys to successful resolution of the COVID pandemic will include:
  • Restoration of careful critical thinking, scientifically sound examination, and healthy dialogue—within the medical community and the public.
  • Massive, honest, and accurate public education—with all citizens doing their homework to the best of their ability.
  • Immediate establishment of panels of fairly selected and internationally respected scientists, scholars, and citizens—an Independent International COVID Commission—to examine and draw best possible conclusions about the questions raised in this article. These panels would model the needed critical thinking, scientifically sound examination, and healthy dialogue that the public would be encouraged to emulate, and their findings would serve as a major source for public education about COVID. The dialogue and deliberations of these panels could be televised for all to see. The public could then determine which individuals and what narratives seem most credible, thoughtful, and scientifically sound.
  • Establishment of scientifically sound COVID data collection—for the first time (at least in the USA) since onset of this pandemic. This includes proper use of PCR testing and confirmation with Sanger sequencing. It also includes scientifically sound diagnostic and classification criteria.
  • Reversal of polarization, demonization, extremism, intolerance, shaming, and censorship.
  • Cessation of media-created excessive fears.
  • Shutdown of the mass vaccination campaign ASAP, out of an abundance of caution, until adequate safety studies have been done.
  • Maximization of optimal outpatient and inpatient treatment for COVID, including assurance that needed medications will be in adequate supply.
  • An open-minded willingness to challenge long-held preferred beliefs and replace those that are lacking truth with more accurate understandings.
  • A new appreciation of and respect for the astonishing genius and competence of the human immune system.
• There is legitimate concern and considerable evidence that SARS-CoV-2 is a bioengineered virus that may have been deliberately unleased on Humanity. It is essential to establish whether this is true, or not, and if true, why and by whom?. If this is true, the decision to do so was most likely made by a collaborative transnational consortium of ultra-wealthy and ultra-powerful individuals (from the USA, China, Europe, and Canada) whose primary concerns and motivations have been preservation of their already enormous power, wealth, and control over the world’s population.

In order to prevent future pandemics and optimally treat victims of the current pandemic: full, impartial, independent, international investigation of the origin of the SARS-CoV-2 virus is imperative.

• The most important conclusion of this article is that an “independent International COVID Commission” is urgently needed to address the questions discussed in this article.

 

*POSTSCRIPT:

The photographs at the beginning of this article are those of Eugene Smith.

W. Eugene Smith (1918-1978) was a brilliant, compassionate photojournalist whose work was most prominently shared in Life magazine during the 1950s and 60s. He cared deeply about issues of war, poverty, justice, suffering, and health. Mostly, he cared about seeking truth, particularly social truths. And he longed for Social Beauty.

About his work, Smith said:

“With considerable soul searching, [and] to the utmost of my ability, I have let truth be the prejudice.

“If I can get them to think, get them to feel, get them to see, then I’ve done about all that I can as a teacher.”

We would all benefit if Eugene Smith were still with us to help us to see, feel, think about, and understand the truths of the COVID pandemic.

Below, I have re-presented the four photos that were presented at the beginning of this article, and I have added captions to them. Those four photos are followed by two additional Smith photos.

 

Robert M. Rennebohm, MD
Pediatrician and Pediatric Rheumatologist
Susac Syndrome Specialist
Email: rmrennebohm@gmail.com
Website: notesfromthesocialclinic.org
September 2021

 

 

If we were to fast-forward from 1950 to 2021 and view this photo in the context of the COVID pandemic, what questions would cross your mind? Are the women mourning a loved one who has died of COVID? Are they mourning his death from COVID but also wondering if his death could have been prevented if he had promptly received better-informed, more aggressive treatment and more compassionate care? Or had he developed a life-threatening non-COVID illness and died because hospital care was less available because of COVID policies? Or are they wondering if he died from a life-threatening adverse reaction to the COVID vaccine? Or do they simply not know what to think, because of the confusion and contentious disagreements regarding COVID?

 

 

If we were to fast-forward from 1950 to 2021 and view this photo in the context of the COVID pandemic, what questions would cross your mind? What is he thinking? Is he thinking about his most recent patient who died of COVID and whether he had done enough to save that patient? Is he wondering what has caused this horrible COVID situation? Is he wondering about the origin of the SARS-CoV-2 virus? Is he wondering whether this pandemic will ever end, whether we will learn enough from it, whether life will ever be the same, whether life will become increasingly worse?

 

 

What is this health care worker thinking? Is she wondering how this COVID pandemic came about, why it has disproportionately affected people of color, why so many small rural hospitals have been closed over the past decade, whether it is best for her and her patients to be vaccinated, whether it is safe to continue to work as a health care worker?

 

 

Is this boy crying because his grandparents have died of COVID? Is he frightened about dying himself? Is he sad that he has missed so much school, has seen so little of his friends, and has not been able to play like before? Is he just very tired of worrying and hearing about COVID and all of the controversies and bad things going on in the world? Is he worried about losing his parents to COVID? Is he saddened because his parents—one a physician, the other a nurse—have lost their jobs because they thought hospital policies were unscientific and harmful to patients? Is he worried about the anxiety and sadness his parents have suffered because of COVID directives? Is he saddened by the cruel and intolerant ways in which people now frequently treat each other? Does he wonder what happened to kindness and compassion? Is he worried that these COVID issues will never end?

 

 

What is this country doctor thinking? Is he wondering how much longer he can continue to attend to all the patients who need him? Is he wondering whether the medications he needs will continue to be available and permitted use? Will there be enough nurses to help him? Are the days of practicing Medicine in the meaningful and rewarding way he had always practiced now over? What does the future hold for Medicine and Humanity?

 

 

This is Albert Schweitzer (1875-1965), hard at work trying to figure out how to best meet his patients’ needs. He was a theologian and philosopher, as well as a physician. In 1952 he was awarded a Nobel Prize for his philosophy of “Reverence for Life.” He devoted his life to caring for patients in Africa, at the Albert Schweitzer Hospital in Lambarene, Gabon. He was one of the first Europeans to believe and act on the notion that African lives mattered. What would Dr. Schweitzer think of the COVID pandemic and how it has been handled—scientifically, ethically, and morally?

 

REFERENCES

1. Ferguson NM, et al. Report 9: Impact of non-pharmaceutical interventions (NPIs) to reduce COVID-19 mortality and healthcare demand. Imperial College COVID-19 Response Team. March 16,2020. DOI: https://doi.org/10.25561/77482
2. Fauci AS, Lane HC, Redfield RR. Covid-19 – Navigating the Uncharted. N Engl J Med. 2020;382(13):1268-1269. doi:10.1056/NEJMe2002387
3. Ioannidis J. Coronavirus disease 2019: The harms of exaggerated information and non-evidence-based measures. Eur J Clin Invest. 2020; March 12.
4. Ioannidis JPA. Infection fatality rate of COVID-19 inferred from seroprevalence data. Bull World Health Organ. 2021;99:19–33F.
5. O’Driscoll M, Dos Santos GR, Wang L, Cummings DAT, Azman AS, Paireau J, et al. Age-specific mortality and immunity patterns of SARS-CoV-2. Nature. 2020.
6. Ioannidis JPA, Axfors C, Contopoulos-Ioannidis DG. Population-level COVID-19 mortality risk for non-elderly individuals overall and for non-elderly individuals without underlying diseases in pandemic epicenters. Environ Res. 2020;188:109890. doi:10.1016/j.envres.2020.109890
7. Axfors C, Ioannides JPA. Infection fatality rate of COVID-19 in community-dwelling populations with emphasis on the elderly: An overview. medRxiv preprint doi: https://doi.org/10.1101/2021.07.08.21260210; this version posted July 13, 2021.
8. Ioannidis JPA. Reconciling estimates of global spread and infection fatality rates of COVID-19: An overview of systematic evaluations. Eur J Clin Invest. 2021;51(5):e13554. doi:10.1111/eci.13554
9. Thornley S, et al. The covid-19 elimination debate needs correct data. BMJ 2020; 371.
10. Baker MG, Wilson N. The covid-19 elimination debate needs correct data. BMJ 2020;371 doi: https://doi.org/10.1136/bmj.m3883
11. CDC; 2020. CDC Estimated Influenza Illnesses, Medical visits, Hospitalizations, and Deaths in the United States — 2017–2018 influenza season. Available at: https://www.cdc.gov/flu/about/burden/2017-2018.htm
12. CDC: Provisional COVID-19 Deaths: Focus on ages 0-18. https://data.cdc.gov/NCHS/Provisional-COVID-19-Deaths-Focus-on-Ages-0-18-Yea/nr4s-juj3
13. Guan WJ, Ni ZY, Hu Y, et al. Clinical Characteristics of Coronavirus Disease 2019 in China. N Engl J Med. 2020;382(18):1708-1720. doi:10.1056/NEJMoa2002032
14. Ackermann M, Verleden SE, Kuehnel M, et al. Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis in Covid-19. N Engl J Med. 2020;383(2):120-128. doi:10.1056/NEJMoa2015432
15. Singhania N, Bansal S, Nimmatoori DP, Ejaz AA, McCullough PA, Singhania G. Current Overview on Hypercoagulability in COVID-19. Am J Cardiovasc Drugs. 2020;20(5):393-403. doi:10.1007/s40256-020-00431-z
16. Bhatt AS, Adler ED, Albert NM, et al. Coronavirus Disease-2019 and Heart Failure: A Scientific Statement from the Heart Failure Society of America [published online ahead of print, 2021 Sep 1]. J Card Fail. 2021;doi:10.1016/j.cardfail.2021.08.013
17. Avolio E, et al. The SARS-CoV-2 spike protein disrupts the cooperative function of human cardiac pericytes-endothelial cells through CD147 receptor-mediated signalling: a potential non-infective mechanism of COVID-19 microvascular disease. bioRxiv preprint doi: https://doi.org/10.1101/2020.12.21.423721
18. Mao L, Jin H, Wang M, Hu Y, Chen S, He Q, Chang J, Hong C, Zhou Y, Wang D, Miao X, Li Y, Hu B. Neurologic manifestations of hospitalized patients with coronavirus disease 2019 in Wuhan, China. JAMA Neurol. 2020;77:683–690. doi: 10.1001/jamaneurol.2020.1127.
19. Camargo-Martínez W, Lozada-Martínez I, Escobar-Collazos A, Navarro-Coronado A, Moscote-Salazar L, Pacheco-Hernández A, Janjua T, Bosque-Varela P. Post-COVID 19 neurological syndrome: implications for sequelae’s treatment. J Clin Neurosci. 2021;88:219–225. doi: 10.1016/j.jocn.2021.04.001.
20. Elmashala A, Chopra S, Garg A. The neurologic manifestations of coronavirus disease 2019. J Neurol Res. 2020;10:107–112. doi: 10.14740/jnr603.
21. Gaddam S. Implications of COVID-19 in neurological disorders. J Neurol Res. 2020;10:160–163. doi: 10.14740/jnr617.
22. Koralnik IJ, Tyler KL. COVID-19: a global threat to the nervous system. Ann Neurol. 2020;88:1–11. doi: 10.1002/ana.25807.
23. Nordvig AS, Fong KT, Willey JZ, Thakur KT, Boehme AK, Vargas WS, Smith CJ, Elkind M. Potential neurologic manifestations of COVID-19. Neurol Clin Pract. 2021;11:e135–135e146. doi: 10.1212/CPJ.0000000000000897.
24. Li X, Wang Y, Wang H, Wang Y. SARS-CoV-2-associated Guillain-Barré syndrome is a para-infectious disease. QJM. 2021 doi: 10.1093/qjmed/hcab157.
25. Keshavarz P, Haseli S, Yazdanpanah F, Bagheri F, Raygani N, Karimi-Galougahi M. A Systematic Review of Imaging Studies in Olfactory Dysfunction Secondary to COVID-19 [published online ahead of print, 2021 Aug 30]. Acad Radiol. 2021;doi:10.1016/j.acra.2021.08.010
26. SARS-CoV-2 variants of concern and variants under investigation in England. Technical briefing 22, Sep 3, 2021. Public Health England. https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/1014926/Technical_Briefing_22_21_09_02.pdf
27. Interview with Dr. Paul Marik: https://www.youtube.com/watch?v=Bkcp04z8pE4
28. Keller MJ, et al. Effects of systemic corticosteroid on mortality or mechanical ventilation in patients with COVID-19. J of Hospital medicine. Published July 22, 2020. Doi:10.12788/jhm.3497
29. Kyriazopoulou, E., Poulakou, G., Milionis, H. et al. Early treatment of COVID-19 with anakinra guided by soluble urokinase plasminogen receptor plasma levels: a double-blind, randomized controlled phase 3 trial. Nat Med (2021). https://doi.org/10.1038/s41591-021-01499-z
30. Chinese Clinical Trial Registry. A multicenter, randomized controlled trial for the efficacy and safety of tocilizumab in the treatment of new coronavirus pneumonia (COVID-19). Feb 13, 2020. http://www.chictr.org.cn/ showprojen.aspx?proj=49409 (accessed March 6, 2020). doi: 10.1016/S0140-6736(20)30628-0. Epub 2020 Mar 16.
31. McGonagle D, Sharif K, O’Regan A, Bridgewood C. Interleukin-6 use in COVID-19 pneumonia related macrophage activation syndrome. Autoimmunity Reviews 2020: 102537. doi: 10.1016/j.autrev.2020.102537
32. Toniati P, Piva S, Cattalini M, et al. Tocilizumab for the treatment of severe COVID-19 pneumonia with hyperinflammatory syndrome and acute respiratory failure: a single center study of 100 patients in Brescia, Italy. Autoimmun Rev 2020; published online May 3. DOI:10.1016/ j. autrev.2020.102568.
33. Zhou W, Liu Y, Tian D, Wang C, Wang S et al. Potential benefits of precise corticosteroids therapy for severe 2019-nCoV pneumonia. Signal Transduction and Targeted Therapy 2020; 5: 18. doi: 10.1038/s41392-020-0127-9
34. Cavalli G, De Luca G, Campochiaro C, et al. Interleukin-1 blockade with high-dose anakinra in patients with COVID-19, acute respiratory distress syndrome, and hyperinflammation: a retrospective cohort study. Lancet Rheumatol 2020; 2: e325–31.
35. Huet T, Beaussier H, Voisin O, et al. Anakinra for severe forms of COVID-19: a cohort study. Lancet Rheumatol 2020; 2: e393–400.
36. Aouba A, Baldolli A, Geffray L, et al. Targeting the inflammatory cascade with anakinra in moderate to severe COVID-19 pneumonia: case series. Ann Rheum Dis 2020; published online May 6. DOI:10.1136/ annrheumdis-2020-217706.
37. Pontali E, Volpi S, Antonucci G, et al. Safety and efficacy of early high-dose IV anakinra in severe COVID-19 lung disease. J Allergy Clin Immunol 2020; published online May 11. DOI:10.1016%2Fj. jaci.2020.05.002.
38. Cao W, Liu X, Bai T, Fan H, Hong K et al. High-dose intravenous immunoglobulin as a therapeutic option for deteriorating patients with coronavirus disease 2019. Open Forum Infectious Diseases. 2020; 7 (3): ofaa102. doi: 10.1093/ ofid/ofaa102
39. Conti P, Gallenga CE, Tete G, Caraffa A, Ronconi G et al. How to reduce the likelihood of coronavirus-19 (CoV-19 or SARSCoV-2) infection and lung inflammation mediated by IL-1. Journal of Biological Regulators and Homeostatic Agents 2020; 34 (2). doi: 10.23812/Editorial-Conti-2
40. Hung IF. Triple combination of interferon beta-1b, lopinavir–ritonavir, and ribavirin in the treatment of patients admitted to hospital with COVID-19: an open-label, randomized, phase 2 trial. Lancet. 2020; May 10.
41. Nile SH, Nile A, Qiu J, et al. COVID-19: Pathogenesis, cytokine storm and therapeutic potential of interferons. Cytokine Growth Factor Rev. 2020; May 7.
42. Shalhoub S. Interferon beta-1b for COVID-19 . Lancet. 2020; May 10.
43. Díez JM, Romero C, Gajardo R. Currently available intravenous immunoglobulin contains antibodies reacting against severe acute respiratory syndrome coronavirus 2 antigens. Immunotherapy. 2020; May 13.
44. Goursaud S. Corticosteroid use in selected patients with severe acute respiratory distress syndrome related to COVID-19 . J Infect. 2020; May 14.
45. Wolhfarth P, Agis H, Gualdoni GA, et al. (2019). Interleukin 1 receptor antagonist anakinra, intravenous immunoglobulin, and corticosteroids in the management of critically ill adult patients with secondary hemophagocytic lymphohistiocytosis. J Intens Care Med. 2019; 34: 723-731.
46. Capra R. Impact of low dose tocilizumab on mortality rate in patients with COVID-19 related pneumonia. Eur J Intern Med. 2020; May 13.
47. Chen P, et al. SARS-CoV-2 Neutralizing Antibody LY-CoV555 in Outpatients with COVID-19. NEJM. October 28, 2020.
48. Vardhana, S.A., and J.D. Wolchok. 2020. The many faces of the anti-COVID immune response. J. Exp. Med. 217:e20200678. https://doi.org/10.1084/ jem.20200678
49. Kuri-Cervantes, L., M.B. Pampena, W. Meng, A.M. Rosenfeld, C.A.G. Ittner, A.R. Weisman, R.S. Agyekum, D. Mathew, A.E. Baxter, L.A. Vella, et al. 2020. Comprehensive mapping of immune perturbations associated with severe COVID-19. Sci. Immunol. 5:eabd7114–20. https://doi.org/10 .1126/sciimmunol.abd7114
50. Silvin, A., N. Chapuis, G. Dunsmore, A.-G. Goubet, A. Dubuisson, L. Derosa, C. Almire, C. Henon, O. Kosmider, N. Droin, et al. 2020. Elevated Cal-protectin and Abnormal Myeloid Cell Subsets Discriminate Severe from Mild COVID-19. Cell. 182:1401–1418.e18. https://doi.org/10.1016/j.cell .2020.08.002
51. Nienhold, R., Y. Ciani, V.H. Koelzer, A. Tzankov, J.D. Haslbauer, T. Menter, N. Schwab, M. Henkel, A. Frank, V. Zsikla, et al. 2020. Two distinct immunopathological profiles in autopsy lungs of COVID-19. Nat. Commun. 11:5086. https://doi.org/10.1038/s41467-020-18854-2
52. Laing, A.G., A. Lorenc, I. Del Molino Del Barrio, A. Das, M. Fish, L. Monin, M. Muñoz-Ruiz, D.R. McKenzie, T.S. Hayday, I. Francos-Quijorna, et al. 2020. A dynamic COVID-19 immune signature includes associations with poor prognosis. Nat. Med. 26:1623–1635. https://doi.org/10.1038/ s41591-020-1038-6
53. Rydyznski Moderbacher, C., S.I. Ramirez, J.M. Dan, A. Grifoni, K.M. Hastie, D. Weiskopf, S. Belanger, R.K. Abbott, C. Kim, J. Choi, et al. 2020. Antigen Specific Adaptive Immunity to SARS-CoV-2 in Acute COVID-19 and Associations with Age and Disease Severity. Cell. 183:996–1012.e19. https://doi.org/10.1016/j.cell.2020.09.038
54. Henderson LA, Canna SW, Schulert GS, et al. On the alert for cytokine storm: immunopathology in COVID-19. Arthritis Rheumatol 2020; published online April 15. DOI:10.1002/art.41285.
55. Qin C, Zhou L, Hu Z, Zhang S, Yang S et al. Dysregulation of immune response in patients with COVID-19 in Wuhan, China. Clinical Infectious Diseases: an official publication of the Infectious Diseases Society of America 2020. doi: 10.1093/ cid/ciaa248
56. Wang W, He J, Lie p, Huang l, Wu S et al. The definition and risks of cytokine release syndrome-like in 11 COVID-19-infected pneumonia critically ill patients: disease characteristics and retrospective analysis. MedRxiv 2020. doi: 10.1101/2020.02.26.20026989
57. Mehta P, McAuley DF, Brown M, Sanchez E, Tattersall RS, Manson JJ. COVID-19: consider cytokine storm syndromes and immunosuppression. Lancet 2020; 395: 1033–34.
58. Channappanavar R, Perlman S. Pathogenic human coronavirus infections: causes and consequences of cytokine storm and immunopathology. Seminars in Immunopathology 2017; 39 (5): 529-539. doi: 10.1007/s00281-017-0629-x
59. Shareef KA, et al. Cytokine Blood Filtration Responses in COVID-19. Blood Purification. Published online: May 28, 2020.
60. Cron RQ, Chatham WW. The rheumatologist’s role in COVID-19. J Rheumatol 2020; 47: 639–42.
61. Halpert G, Shoenfeld Y. SARS-CoV-2, the autoimmune virus. Autoimmunity Reviews 19 (2020) 102695. https://doi.org/10.1016/j.autrev.2020.102695
62. Shoenfeld Y. Corona (COVID-19) time musings: Our involvement in COVID-19 pathogenesis, diagnosis, treatment and vaccine planning. Autoimmunity Reviews 19 (2020) 102538. https://doi.org/10.1016/j.autrev.2020.102538
63. Ruscitti P, Berardicurti O, Di Benedetto P, et, al. (2020) Severe COVID-19, Another Piece in the Puzzle of the Hyperferritinemic Syndrome. An Immunomodulatory Perspective to Alleviate the Storm. Front. Immunol. 11:1130. doi: 10.3389/fimmu.2020.01130
64. Ryabkova VA, Churilov LP, Shoenfeld Y. Influenza infection, SARS, MERS and COVID-19: Cytokine storm – The common denominator and the lessons to be learned. Clinical Immunology 223 (2021) 108652 https://doi.org/10.1016/j.clim.2020.108652
65. Rennebohm RM. Has undertreatment of severe COVID illness been widespread? A pediatric rheumatologist’s perspective. Russia Biomedical Research, 2020, Vol 5, No 3, p. 3-13.
66. McCullough PA, Kelly RJ, Ruocco G, et al. Pathophysiological Basis and Rationale for Early Outpatient Treatment of SARS-CoV-2 (COVID-19) Infection. Am J Med. 2021;134(1):16-22. doi:10.1016/j.amjmed.2020.07.003
67. Prevention and Treatment Protocols for COVID-19. FLCCC Alliance: https://covid19criticalcare.com/covid-19-protocols/
68. Bryant A, Lawrie TA, Dowswell T, et al. Ivermectin for Prevention and Treatment of COVID-19 Infection: A Systematic Review, Meta-analysis, and Trial Sequential Analysis to Inform Clinical Guidelines. Am J Ther. 2021;28(4):e434-e460. Published 2021 Jun 21. doi:10.1097/MJT.0000000000001402
69. Kory P, Meduri GU, Varon J, Iglesias J, Marik PE. Review of the Emerging Evidence Demonstrating the Efficacy of Ivermectin in the Prophylaxis and Treatment of COVID-19. Am J Ther. 2021 Apr 22;28(3):e299-e318. doi: 10.1097/MJT.0000000000001377. PMID: 34375047; PMCID: PMC8088823.
70. Jans DA, Wagstaff KM. The broad-spectrum host-directed agent ivermectin as an antiviral for SARS-CoV-2 ? Biochem Biophys Res Commun. 2021 Jan 29;538:163-172. doi: 10.1016/j.bbrc.2020.10.042. Epub 2020 Oct 21. PMID: 33341233; PMCID: PMC7577703.
71. Alexander PE, Armstrong R, Fareed G, et al. Early multidrug treatment of SARS-CoV-2 infection (COVID-19) and reduced mortality among nursing home (or outpatient/ambulatory) residents. Med Hypotheses. 2021;153:110622. doi:10.1016/j.mehy.2021.110622
72. Santin AD, Scheim DE, McCullough PA, Yagisawa M, Borody TJ. Ivermectin: a multifaceted drug of Nobel prize-honoured distinction with indicated efficacy against a new global scourge, COVID-19. New Microbes New Infect. 2021;43:100924. Published 2021 Aug 3. doi:10.1016/j.nmni.2021.100924
73. McCullough PA, Oskoui R. Early multidrug regimens in new potentially fatal medical problems. Rev Cardiovasc Med. 2020;21(4):507–508.
74. Procter BC, Ross C, Pickard V, Smith E, Hanson C, McCullough PA. Clinical outcomes after early ambulatory multidrug therapy for high-risk SARS-CoV-2 (COVID-19) infection. Rev Cardiovasc Med. 2020;21(4):611–614.
75. Procter BC, Ross C, Pickard V, Smith E, Hanson C, McCullough PA. Early ambulatory multidrug therapy reduces hospitalization and death in high-risk patients with SARS-CoV-2 (COVID-19) Authorea. January 07, 2021 doi: 10.22541/au.161000355.54720791/v1.
76. McCullough PA, Alexander PE, Armstrong R. Multifaceted highly targeted sequential multidrug treatment of early ambulatory high-risk SARS-CoV-2 infection (COVID-19) Rev Cardiovasc Med. 2020;21(4):517–530.
77. McCullough PA. Regarding: “Hydroxychloroquine: a comprehensive review and its controversial role in coronavirus disease 2019”. Ann Med. 2021;53(1):286. doi:10.1080/07853890.2021.1872094
78. McCullough PA. Favipiravir and the Need for Early Ambulatory Treatment of SARS-CoV-2 Infection (COVID-19). Antimicrob Agents Chemother. 2020;64(12):e02017-20. Published 2020 Nov 17. doi:10.1128/AAC.02017-20
79. Derwand R, Scholz M, Zelenko V. COVID-19 outpatients: early risk-stratified treatment with zinc plus low-dose hydroxychloroquine and azithromycin: a retrospective case series study. Int J Antimicrob Agents. 2020;56(6):106214. doi:10.1016/j.ijantimicag.2020.106214
80. Cobos-Campos R, Apiñaniz A, Parraza N, Cordero J, García S, Orruño E. Potential use of ivermectin for the treatment and prophylaxis of SARS-CoV-2 infection [published online ahead of print, 2021 Aug 11]. Curr Res Transl Med. 2021;69(4):103309. doi:10.1016/j.retram.2021.103309
81. Ngo BT, Marik P, Kory P, et al. The time to offer treatments for COVID-19. Expert Opin Investig Drugs. 2021;30(5):505-518. doi:10.1080/13543784.2021.1901883
82. Kory P, Kanne JP. SARS-CoV-2 organising pneumonia: ‘Has there been a widespread failure to identify and treat this prevalent condition in COVID-19?’. BMJ Open Respir Res. 2020;7(1):e000724. doi:10.1136/bmjresp-2020-000724
83. Cavalli E, Bramanti A, Ciurleo R, et.al. Entangling COVID-19 associated thrombosis into a secondary antiphospholipid antibody syndrome: Diagnostic and therapeutic perspectives (Review). International Journal of Molecular Medicine. DOI: 10.3892/ijmm.2020.4659
84. Rennebohm RM. Analysis of the COVID-19 epidemic: an additional narrative; an alternative response. Pediatrician (St. Petersburg). 2020;11(3):23-40. https://doi.org/10.17816/PED11323-40
85. Centers for Disease Control and Prevention. Coronavirus disease (2019). Interim clinical guidance for management of patients with confirmed coronavirus disease (COVID-19). March 2020. URL: https://www.cdc.gov/coronavirus/2019-ncov/hcp/clinical-guidancemanagement-patients.html#clinical-management-treatment%3C.
86. Bhimraj A. Infectious Diseases Society of America Guidelines on the Treatment and Management of Patients with COVID-19 . Clin Infect Dis. 2020; Apr 27.
87. Nicastri E. National Institute for the Infectious Diseases “L. Spallanzani,” IRCCS. Recommendations for COVID-19 clinical management. Infectious Disease Reports. 2020; 12: 8543.
88. Covid19treatmentguidelines.nih.gov
89. Binnicker MJ. 2020. Challenges and controversies to testing for COVID-19. J Clin Microbiol 58: e01695-20. https://doi.org/10 .1128/JCM.01695-20
90. Tom MR, Mina MJ. To Interpret the SARS-CoV-2 Test, Consider the Cycle Threshold Value. Clin Infect Dis. 2020 May 21: ciaa619. Published online 2020 May 21. doi: 10.1093/cid/ciaa619
91. Hosseini A, Pandey R, Osman E, et al. Roadmap to the Bioanalytical Testing of COVID-19: From Sample Collection to Disease Surveillance [published online ahead of print, 2020 Oct 30]. ACS Sens. 2020; acssensors.0c01377. doi:10.1021/acssensors.0c01377
92. Guo JJ, Yu YH, Ma XY, et al. A multiple-center clinical evaluation of a new real-time reverse transcriptase PCR diagnostic kit for SARS-CoV-2. Future Virol. 2020;10.2217/fvl-2020-0299. doi:10.2217/fvl-2020-0299
93. Wang M, Chen D, Wu W, et al. Analytical performance evaluation of five RT-PCR kits for severe acute respiratory syndrome coronavirus 2 [published online ahead of print, 2020 Oct 27]. J Clin Lab Anal. 2020; e23643. doi:10.1002/jcla.23643
94. Yüce M, Filiztekin E, Özkaya KG. COVID-19 diagnosis -A review of current methods [published online ahead of print, 2020 Oct 24]. Biosens Bioelectron. 2020; 172:112752. doi:10.1016/j.bios.2020.112752
95. Your Coronavirus Test is Positive. Maybe it shouldn’t be. Interview with Michael Mina, MD. Published August 29, 2020; Updated September 17, 2020. https://www.nytimes.com/2020/08/29/health/coronavirus-testing.html
96. Vandenberg O, et al. Considerations for diagnostic COVID-19 tests. Nat Rev Microbiol. 2020 Oct 14: 1–13. doi: 10.1038/s41579-020-00461-z
97. Surkova E, et al. False-positive COVID-19 results: hidden problems and costs. Lancet Resp Med. published online, September 29, 2020. https://doi.org/10.1016/52213-2600(20)30453-7
98. Mayers C, Baker K. Impact of false-positives and false-negatives in the UK’s COVID-19 RT-PCR testing programme. June 3, 2020. https://assets. publishing.service.gov.uk/government/uploads/system/uploads/ attachment_data/file/895843/S0519_Impact_of_false_positives_and_ negatives.pdf (accessed Aug 8, 2020).
99. Skittrall JP, Wilson M, Smielewska AA, et al. Specificity and positive predictive value of SARS-CoV-2 nucleic acid amplification testing in a low-prevalence setting [published online ahead of print, 2020 Oct 14]. Clin Microbiol Infect. 2020; S1198-743X (20)30614-5. doi:10.1016/j.cmi.2020.10.003
100. Hellou MM, et al Nucleic-acid-amplification tests from respiratory samples for the diagnosis of coronavirus infections: systematic review and meta-analysis, Clinical Microbiology and Infection, https://doi.org/10.1016/j.cmi.2020.11.002.
101. Corman VM, Landt O, Kaiser M, et al. Detection of 2019 Novel Coronavirus (2019-NCoV) by Real-Time RT-PCR. Euro Surveill. 2020, 25 (3), 1−8.
102. Corman V B, leicker T, Brunink S, et al. Diagnostic Detection of Wuhan Coronavirus 2019 by Real-Time RT-PCR; World Health Organization, 2020; pp 1−12.
103. Francesca F, et al. Detection of SARS-COV N2 Gene: Very low amounts of viral RNA or false positive? J Clin Virol. 2020 Dec; 133: 104660. Published online 2020 Oct 14. https://doi.org/10.1016/j.jcv.2020.104660
104. Katz AP, et al. False positive reverse transcriptase polymerase chain reaction screening for SARS-CoV-2 in the setting of urgent head and neck surgery and otolaryngologic emergencies during the pandemic: Clinical implications, Head Neck 42 (7) (2020) 1621–1628, https://doi.org/10.1002/hed.26317
105. Wang Z, et al. External Quality Assessment for Molecular Detection of Severe Acute Respiratory Syndrome Coronavirus 2 in Clinical laboratories, The Journal of Molecular Diagnostics (2020), doi: https://doi.org/10.1016/j.jmoldx.2020.10.008.
106. Cohen AN, et al. Diagnosing SARS-CoV-2 infection: the danger of over-reliance on positive test results; false positive test results impact clinical and policy decisions. medRxiv preprint doi: https://doi.org/10.1101/2020.04.26.20080911
107. Cohen AN, Kessel B, Milgroom MG. Analysis of expected false positive rates in SARS-CoV-2 testing: technical background, limitations and objections. https://doi.org/10.5281/zenodo.4035317.
108. Ruiz-Villalba A, et al. Amplification of nonspecific products in quantitative polymerase chain reactions (qPCR) Biomol Detect Quantif. 2017 Dec; 14: 7–18. Published online 2017 Nov 1. doi: 10.1016/j.bdq.2017.10.001
109. Willman D. Contamination at CDC lab delayed rollout of coronavirus tests. April 18, 2020. https://www.washingtonpost.com/investigations/ contamination-at-cdc-lab-delayed-rollout-of-coronavirustests/2020/04/18/fd7d3824-7139-11ea-aa80-c2470c6b2034_story.html. (accessed Aug 16, 2020).
110. Bullard J, et al. Predicting infectious SARS-CoV-2 from diagnostic samples. Clin Infect Dis. 2020 May 22: ciaa638. Published online 2020 May 22. doi: 10.1093/cid/ciaa638
111. Singanayagam A, Patel M, Charlett A, et al. (2020). Duration of infectiousness and correlation with RT-PCR cycle threshold values in cases of COVID-19, England, January to May 2020. Euro surveillance: bulletin Europeen sur les maladies transmissibles = European communicable disease bulletin, 25(32), 2001483. https://doi.org/10.2807/1560-7917.ES.2020.25.32.2001483
112. Jaafar R, Aherfi S, Wurtz N, et al. Correlation Between 3790 Quantitative Polymerase Chain Reaction–Positives Samples and Positive Cell Cultures, Including 1941 Severe Acute Respiratory Syndrome Coronavirus 2 Isolates, Clinical Infectious Diseases, ciaa1491, https://doi.org/10.1093/cid/ciaa1491
113. Ivanova E, et al. Discrete Immune Response Signature to SARS-CoV-2 mRNA Vaccination Versus Infection. Available at SSRN: https://ssrn.com/abstract=3838993 or http://dx.doi.org/10.2139/ssrn.3838993
114. Sekine, T. et al. Robust T cell immunity in convalescent individuals with asymptomatic or mild COVID-19. Cell https://doi.org/10.1016/j.cell.2020.08.017 (2020).
115. Nielsen, S.S. et al. (2021) SARS-CoV-2 elicits robust adaptive immune responses regardless of disease severity. EBioMedicine 68:103410
116. Gallais, F. et al. (2021) Intrafamilial Exposure to SARS-CoV-2 Associated with Cellular Immune Response without Seroconversion. Emerg. Infect. Dis. 27 (preprint)
117. Grifoni, A. et al. (2020) Targets of T Cell Responses to SARS-CoV-2 Coronavirus in Humans with COVID-19 Disease and Unexposed Individuals. Cell 181:1489-1501.e15
118. Le Bert, N. et al. (2020) SARS-CoV-2-specific T cell immunity in cases of COVID-19 and SARS, and uninfected controls. Nature 584:457-462
119. Qu, J. et al. (2020) Profile of Immunoglobulin G and IgM Antibodies Against Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). Clin. Infect. Dis. 71:2255-2258
120. Turner, J.S., Ki, W., Kalaidina, E. et al. SARS-CoV-2 infection induces long-lived bone marrow plasma cells in humans. Nature 595, 421–425 (2021). https://doi.org/10.1038/s41586-021-03647-4
121. Shrestha NK, et al. Necessity of COVID-19 vaccination in previously infected individuals. medRxiv 2021.06.01.21258176; doi: https://doi.org/10.1101/2021.06.01.21258176
122. Cohen KW, et al. Longitudinal analysis shows durable and broad immune memory after SARS-CoV-2 infection with persisting antibody responses and memory B and T cells. Cell Reports Medicine; 2, 100354, July 20, 2021. DOI: https://doi.org/10.1016/j.xcrm.2021.100354
123. Murchu EO, et al. Quantifying the risk of SARS‐CoV‐2 reinfection over time. Rev Med Virol. 2021;e2260. https://doi.org/10.1002/rmv.2260
124. Abu-Raddad LJ, et al. SARS-CoV-2 antibody-positivity protects against reinfection for at least seven months with 95% efficacy. EClinicalMedicine 35 (2021) 100861. https://doi.org/10.1016/j.eclinm.2021.100861
125. Goldberg Y, et al. Protection of previous SARS-CoV-2 infection is similar to that of BNT162b2 vaccine protection: A three-month nationwide experience from Israel. medRxiv preprint doi: https://doi.org/10.1101/2021.04.20.21255. doi: https://doi.org/10.1101/2021.04.20.21255670
126. Gonzalez C, et al. Live virus neutralisation testing in convalescent patients and subjects vaccinated against 19A, 20B, 20I/501Y.V1 and 20H/501Y.V2 isolates of SARS-CoV-2. medRxiv preprint doi: https://doi.org/10.1101/2021.05.11.21256578
127. LeBert N, et al. Highly functional virus-specific cellular immune response in asymptomatic SARS-CoV-2 infection. J Exp Med (2021) 218 (5): e20202617.https://doi.org/10.1084/jem.20202617
128. Jung, JH, et al. SARS-CoV-2-specific T cell memory is sustained in COVID-19 convalescent patients for 10 months with successful development of stem cell-like memory T cells. Nat Commun 12, 4043 (2021). https://doi.org/10.1038/s41467-021-24377-1
129. Camara C, et al. Differential effects of the second SARS-CoV-2 mRNA vaccine dose on T cell immunity in naïve and COVID-19 recovered individuals. bioRxiv preprint doi: https://doi.org/10.1101/2021.03.22.436441
130. Ng, O. W. et al. Memory T cell responses targeting the SARS coronavirus persist up to 11 years post-infection. Vaccine 34, 2008–2014 (2016).
131. Zhao, J. X. et al. Recovery from the Middle East respiratory syndrome is associated with antibody and T cell responses. Sci. Immunol. 2, eaan5393 (2017).
132. Dan, J. M. et al. Immunological memory to SARS-CoV-2 assessed for up to 8 months after infection. Science 371, eabf4063 (2021).
133. Tseng, C. T., Sbrana, E., Iwata-Yoshikawa, N., Newman, P. C., Garron, T., Atmar, R. L., Peters, C. J., & Couch, R. B. (2012). Immunization with SARS coronavirus vaccines leads to pulmonary immunopathology on challenge with the SARS virus. PloS one, 7(4), e35421. https://doi.org/10.1371/journal.pone.0035421
134. Haagmans BL, Boudet F, Kuiken T, deLang A, Martina BE, et al. (2005) Protective immunity induced by the inactivated SARS coronavirus vaccine. Abstract S 12-1. Presented at the X International Nidovirus Symposium, Colorado Springs, CO.
135. Castilow EM, Olson MR, Varga SM (2007) Understanding respiratory syncytial virus (RSV) vaccine-enhanced disease. Immunol Res 39: 225–239. 33.
136. Collins PL, Graham BS (2008) Viral and host factors in human respiratory syncytial virus pathogenesis. J Virol 82: 2040–2055.
137. Weiss RC, Scott FW (1981) Antibody-mediated enhancement of disease in feline infectious peritonitis: comparisons with dengue hemorrhagic fever. Comp Immunol Microbiol Infect Dis 4: 175–89.
138. Kim HW, Canchola JG, Brandt CD, Pyles G, Chanock RM, et al. (1969) Respiratory syncytial virus disease in infants despite prior administration of antigenic inactivated vaccine. Am J Epidemiol 89: 422–34. 42.
139. Waris ME, Tsou C, Erdman DD, Zaki SR, Anderson LJ (1996) Respiratory syncytial virus infection in BALB/c mice previously immunized with formalin inactivated virus induces enhanced pulmonary inflammatory response with a predominant Th2-like cytokine pattern. J Virol 70: 2852–60. 43.
140. Polack FP, Teng MN, Collins PL, Prince GA, Exner M, et al. (2002) A role for immune complexes in enhanced respiratory syncytial virus disease. J Exp Med 196: 859–65.
141. Dolton G, et al. Emergence of immune escape at dominant SARS-CoV-2 killer T-cell epitope. medRxiv preprint doi: https://doi.org/10.1101/2021.06.21.21259010
142. Martin DP, et al. (2021). The emergence and ongoing convergent evolution of the N501Y lineages coincides with a major global shift in the SARS-CoV-2 selective landscape. medRxiv : the preprint server for health sciences, 2021.02.23.21252268. https://doi.org/10.1101/2021.02.23.21252268
143. Van Egeren D, et al. (2021) Risk of rapid evolutionary escape from biomedical interventions targeting SARS-CoV-2 spike protein. PLOS ONE 16(4): e0250780. https://doi.org/10.1371/journal.pone.0250780
144. Harvey WT, et al. SARS-CoV-2 variants, spike mutations and immune escape. Nature Reviews/Microbiology. Vol 19, July, 2021, 409. https://www.nature.com/articles/s41579-021-00573-0.pdf
145. Restif O, Grenfell BT. Vaccination and the dynamics of immune evasion. J R Soc Interface. 2007 Feb 22;4(12):143-53. doi: 10.1098/rsif.2006.0167. PMID: 17210532; PMCID: PMC2358969.
146. Zhou D, et al., Evidence of escape of SARS-CoV-2 variant B.1.351 from natural and vaccine-induced sera. Cell 189, 2348–2361 April 29, 2021. https://doi.org/10.1016/j.cell.2021.02.037
147. Read AF, Baigent SJ, Powers C, Kgosana LB, Blackwell L, et al. (2015) Imperfect Vaccination Can Enhance the Transmission of Highly Virulent Pathogens. PLOS Biology 13(7): e1002198. https://doi.org/10.1371/journal.pbio.1002198
148. Atlani-Duault L, et al. Immune evasion means we need a new COVID-19 social contract. The Lancet Public Health. Vol 6, issue 4, E199-E200, April 1, 2021. https://doi.org/10.1016/ S2468-2667(21)00036-0
149. Karim SSA. Vaccines and SARS-CoV-2 variants: the urgent need for a correlate of protection. The Lancet; March 22, 2021. https://doi.org/10.1016/S0140-6736(21)00468-2
150. Liu Y, et al. The SARS-CoV-2 Delta variant is poised to acquire complete resistance to wild-type spike vaccines. bioRxiv preprint doi: https://doi.org/10.1101/2021.08.22.457114
151. Lee, W.S., Wheatley, A.K., Kent, S.J. et al. Antibody-dependent enhancement and SARS-CoV-2 vaccines and therapies. Nat Microbiol 5, 1185–1191 (2020). https://doi.org/10.1038/s41564-020-00789-5
152. Lyons-Weiler J. Pathogenic priming likely contributes to serious and critical illness and mortality in COVID-19 via autoimmunity. Journal of Translational Autoimmunity 3 (2020) 100051. https://doi.org/10.1016/j.jtauto.2020.100051
153. Yahi N, Chahinian H, Fantini J. Infection-enhancing anti-SARS-CoV-2 antibodies recognize both the original Wuhan / D614G strain and Delta variants. A potential risk for mass vaccination? J Infect. 2021 Aug 9: S0163-4453 (21) 00392-3.
154. Ulrich H, Pillat MM, Tárnok A. Dengue Fever, COVID-19 (SARS-CoV-2), and Antibody-Dependent Enhancement (ADE): A Perspective. Cytometry A. 2020 Jul; 97 (7): 662-667.
155. Cardozo T, Veazey R. Informed consent disclosure to vaccine trial subjects of risk of COVID-19 vaccines worsening clinical disease. Int J Clin Pract. 2021 Mar; 75 (3): e13795.
156. Hohdatsu, T. et al. Antibody-dependent enhancement of feline infectious peritonitis virus infection in feline alveolar macrophages and human monocyte cell line U937 by serum of cats experimentally or naturally infected with feline coronavirus. J. Vet. Med. Sci. 60, 49–55 (1998).
157. Halstead, S. B. & O’Rourke, E. J. Dengue viruses and mononuclear phagocytes. I. Infection enhancement by non-neutralizing antibody. J. Exp. Med. 146, 201–217 (1977).
158. Vennema, H. et al. Early death after feline infectious peritonitis virus challenge due to recombinant vaccinia virus immunization. J. Virol. 64, 1407–1409 (1990).
159. Hohdatsu, T., Nakamura, M., Ishizuka, Y., Yamada, H. & Koyama, H. A study on the mechanism of antibody-dependent enhancement of feline infectious peritonitis virus infection in feline macrophages by monoclonal antibodies. Arch. Virol. 120, 207–217 (1991).
160. Ye, Z. W. et al. Antibody-dependent cell-mediated cytotoxicity epitopes on the hemagglutinin head region of pandemic H1N1 influenza virus play detrimental roles in H1N1-infected mice. Front. Immunol. 8, 317 (2017).
161. Winarski, K. L. et al. Antibody-dependent enhancement of influenza disease promoted by increase in hemagglutinin stem flexibility and virus fusion kinetics. Proc. Natl Acad. Sci. USA 116, 15194–15199 (2019).
162. Gao, T. et al. Highly pathogenic coronavirus N protein aggravates lung injury by MASP-2-mediated complement over-activation. Preprint at https://www.medrxiv.org/content/10.1101/2020.03.29.20041962v3 (2020).
163. Gralinski, L. E. et al. Complement activation contributes to severe acute respiratory syndrome coronavirus pathogenesis. mBio 9, e01753-18 (2018).
164. Wang, T. T. et al. IgG antibodies to dengue enhanced for FcγRIIIA binding determine disease severity. Science 355, 395–398 (2017).
165. Yip, M. S. et al. Antibody-dependent infection of human macrophages by severe acute respiratory syndrome coronavirus. Virol. J. 11, 82 (2014).
166. Takada, A., Watanabe, S., Okazaki, K., Kida, H. & Kawaoka, Y. Infectivity-enhancing antibodies to Ebola virus glycoprotein. J. Virol. 75, 2324–2330 (2001).
167. Takada, A., Feldmann, H., Ksiazek, T. G. & Kawaoka, Y. Antibody-dependent enhancement of Ebola virus infection. J. Virol. 77, 7539–7544 (2003).
168. Ochiai, H. et al. Infection enhancement of influenza A NWS virus in primary murine macrophages by anti-hemagglutinin monoclonal antibody. J. Med. Virol. 36, 217–221 (1992).
169. Wan, Y. et al. Molecular mechanism for antibody-dependent enhancement of coronavirus entry. J. Virol. 94, e02015-19 (2020).
170. Jaume, M. et al. Anti-severe acute respiratory syndrome coronavirus spike antibodies trigger infection of human immune cells via a pH- and cysteine protease-independent FcγR pathway. J. Virol. 85, 10582–10597 (2011).
171. Cheung, C. Y. et al. Cytokine responses in severe acute respiratory syndrome coronavirus-infected macrophages in vitro: possible relevance to pathogenesis. J. Virol. 79, 7819–7826 (2005).
172. Yip, M. S. et al. Antibody-dependent enhancement of SARS coronavirus infection and its role in the pathogenesis of SARS. Hong Kong Med. J. 22, 25–31 (2016).
173. Ana-Sosa-Batiz, F. et al. Influenza-specific antibody-dependent phagocytosis. PLoS ONE 11, e0154461 (2016).
174. Bolles, M. et al. A double-inactivated severe acute respiratory syndrome coronavirus vaccine provides incomplete protection in mice and induces increased eosinophilic proinflammatory pulmonary response upon challenge. J. Virol. 85, 12201–12215 (2011).
175. Yasui, F. et al. Prior immunization with severe acute respiratory syndrome (SARS)-associated coronavirus (SARS-CoV) nucleocapsid protein causes severe pneumonia in mice infected with SARS-CoV. J. Immunol. 181, 6337–6348 (2008).
176. Agrawal, A. S. et al. Immunization with inactivated Middle East respiratory syndrome coronavirus vaccine leads to lung immunopathology on challenge with live virus. Hum. Vaccin. Immunother. 12, 2351–2356 (2016).
177. Weingartl, H. et al. Immunization with modified vaccinia virus Ankara-based recombinant vaccine against severe acute respiratory syndrome is associated with enhanced hepatitis in ferrets. J. Virol. 78, 12672–12676 (2004).
178. Liu, L. et al. Anti-spike IgG causes severe acute lung injury by skewing macrophage responses during acute SARS-CoV infection. JCI Insight 4, e123158 (2019).
179. Luo, F. et al. Evaluation of antibody-dependent enhancement of SARS-CoV infection in rhesus macaques immunized with an inactivated SARS-CoV vaccine. Virol. Sin. 33, 201–204 (2018).
180. Carsetti R, Quintarelli C, Quinti I, et al. The immune system of children: the key to understanding SARS-CoV-2 susceptibility?. Lancet Child Adolesc Health. 2020;4(6):414-416. doi:10.1016/S2352-4642(20)30135-8
181. Holodick NE, Rodríguez-Zhurbenko N, Hernández AM. Defining Natural Antibodies. Front Immunol. 2017;8:872. [PMC free article] [PubMed] [Google Scholar]
182. Ochsenbein AF, Fehr T, Lutz C. Control of early viral and bacterial distribution and disease by natural antibodies. Science. 1999;286:2156–2159. [PubMed] [Google Scholar]
183. Karikó, K., Muramatsu, H., Welsh, F. A., Ludwig, J., Kato, H., Akira, S., & Weissman, D. (2008). Incorporation of pseudouridine into mRNA yields superior nonimmunogenic vector with increased translational capacity and biological stability. Molecular therapy : the journal of the American Society of Gene Therapy, 16(11), 1833–1840. https://doi.org/10.1038/mt.2008.200
184. Mulligan, M.J., Lyke, K.E., Kitchin, N. et al. Publisher Correction: Phase I/II study of COVID-19 RNA vaccine BNT162b1 in adults. Nature 590, E26 (2021). https://doi.org/10.1038/s41586-020-03098-3
185. Ogata AF, Cheng CA, Desjardins M, Senussi Y, Sherman AC, Powell M, Novack L, Von S, Li X, Baden LR, Walt DR. Circulating SARS-CoV-2 Vaccine Antigen Detected in the Plasma of mRNA-1273 Vaccine Recipients. Clin Infect Dis. 2021 May 20: ciab465.
186. https://childrenshealthdefense.org/defender/covid-vaccine-spike-protein-travels-from-injection-site-organ-damage/ (Byram Bridle)
187. https://www.nytimes.com/2021/01/12/health/covid-vaccine-death.html
188. Kanduc, D., Shoenfeld, Y. Molecular mimicry between SARS-CoV-2 spike glycoprotein and mammalian proteomes: implications for the vaccine. Immunol Res 68, 310–313 (2020). https://doi.org/10.1007/s12026-020-09152-6
189. Shoenfeld Y. Corona (COVID-19) time musings: Our involvement in COVID-19 pathogenesis, diagnosis, treatment and vaccine planning. Autoimmunity Reviews 19 (2020) 102538. https://doi.org/10.1016/j.autrev.2020.102538
190. Ehrenfeld M, et al., Autoimmunity Reviews, https://doi.org/10.1016/j.autrev.2020.102597
191. Zhang S, Liu Y, Wang X, Yang L, Li H, Wang Y, Liu M, Zhao X, Xie Y, Yang Y, Zhang S, Fan Z, Dong J, Yuan Z, Ding Z, Zhang Y, Hu L SARS-CoV-2 binds platelet ACE2 to enhance thrombosis in COVID-19. J Hematol Oncol. 2020 Sep 4; 13 (1): 120.
192. Greinacher A, Thiele T, Warkentin TE, Weisser K, Kyrle PA, Eichinger S. Thrombotic Thrombocytopenia after ChAdOx1 nCov-19 Vaccination. N Engl J Med. 2021 Jun 3; 384 (22): 2092-2101.
193. Hermans C, Goldman M. Thrombosis and vaccines: a new challenge in the COVID-19 pandemic. Louvain Med 2021 Apr: 140: 207-215.
194. Long B, Bridwell R, Gottlieb M. Thrombosis with thrombocytopenia syndrome associated with COVID-19 vaccines. Am J Emerg Med. 2021 May 25; 49: 58-61.
195. Lei Y, Zhang J, Schiavon CR, He M, Chen L, Shen H, Zhang Y, Yin Q, Cho Y, Andrade L, Shadel GS, Hepokoski M, Lei T, Wang H, Zhang J, Yuan JX, Malhotra A , Manor U, Wang S, Yuan ZY, Shyy JY. SARS-CoV-2 Spike Protein Impairs Endothelial Function via Downregulation of ACE 2. Circ Res. 2021 Apr 30; 128 (9): 1323-1326.
196. Nuovo GJ, Magro C, Shaffer T, Awad H, Suster D, Mikhail S, He B, Michaille JJ, Liechtenstein B, Tili E. Endothelial cell damage is the central part of COVID-19 and a mouse model induced by injection of the S1 subunit of the spike protein. Ann Diagn Pathol. 2021 Apr; 51: 151682.
197. Buzhdygana, TP, DeOrec, BJ, Baldwin-Leclair, A., Bullock, TA, McGary, H. M, Ramirez, SH (2020). The SARS-CoV-2 Spike Protein Alters Barrier Function in 2D Static and 3D Microfluidic in-Vitro Models of the Human Blood-Brain Barrier. Neurobiology of Disease 146: 105131.
198. Rhea EM, Logsdon AF, Hansen KM et al. The S1 Protein of SARS-CoV-2 Crosses the Blood-Brain Barrier in Mice. Nature Neuroscience 2021; 24: 368-378.
199. Konstantinidis I, Tsakiropoulou E, Hähner A, de With K, Poulas K, Hummel T. Olfactory dysfunction after coronavirus disease 2019 (COVID-19) vaccination. Int Forum Allergy Rhinol. 2021 May 28: 10.1002 / alr. 22809.
200. Biancatelli RMLC, et al. The SARS-CoV-2 spike protein subunit S1 induces COVID-19-like acute lung injury in K18-hACE2 transgenic mice and barrier dysfunction in human endothelial cells Am J Physiol Lung Cell Mol Physiol 321: L477–L484, 2021
201. Diaz GA, Parsons GT, Gering SK, Meier AR, Hutchinson IV, Robicsek A. Myocarditis and Pericarditis After Vaccination for COVID-19. JAMA. 2021 Aug 4.
202. Dionne A, Sperotto F, Chamberlain S, et al. Association of Myocarditis With BNT162b2 Messenger RNA COVID-19 Vaccine in a Case Series of Children. JAMA Cardiol. Published online August 10, 2021.
203. Bril F, Al Diffalha S, Dean M, Fettig DM. Autoimmune hepatitis developing after coronavirus disease 2019 (COVID-19) vaccine: Causality or casualty? J Hepatol. 2021 Jul; 75 (1): 222-224.
204. Rela M, Jothimani D, Vij M, Rajakumar A, Rammohan A. Autoimmune hepatitis following COVID vaccination. J Autoimmun. 2021 Jul 3; 123: 102688.
205. Rocco A, Sgamato C, Compare D, Nardone G. Autoimmune hepatitis following SARS-CoV-2 vaccine: May not be a casualty. J Hepatol. 2021 Jun 9: S0168-8278 (21) 00412-8.
206. Seneff S and Nigh G. Worse Than the Disease? Reviewing Some Possible Unintended Consequences of the mRNA Vaccines. International Journal of Vaccine Theory, Practice, and Research 2 (1), May 10, 2021 Page | 38
207. Suzuki YJ, Gychka SG. SARS-CoV-2 Spike Protein Elicits Cell Signaling in Human Host Cells: Implications for Possible Consequences of COVID-19 Vaccines. Vaccines (Basel). 2021 Jan 11; 9 (1): 36.
208. Angeli F, Spanevello A, Reboldi G, Visca D, Verdecchia P. SARS-CoV-2 vaccines: Lights and shadows. Eur J Intern Med. 2021 Jun; 88: 1-8.
209. Klein NP, et al. Surveillance for adverse events after COVID-19 mRNA vaccination. JAMA. Published September 3, 2021. doi:10.1001/jama.2021.15072
210. Rose J. VAERS Update: Presentation for the Canadian Covid Care Alliance. https://www.youtube.com/watch?v=Y4MViwU3XOo
211. CDC Report, September 2, 2021: Selected Adverse Events Reported after COVID-19 Vaccination. https://www.cdc.gov/coronavirus/2019-ncov/vaccines/safety/adverse-events.html
212. National Vaccine Information Center: https://www.medalerts.org/vaersdb/findfield.php?TABLE=ON&GROUP1=AGE&EVENTS=ON&VAX=COVID19&DIED=Yes
213. Public Health Ontario: Advanced Epidemiological Summary. Myocarditis and Pericarditis Following Vaccination with COVID-19 mRNA Vaccines in Ontario: December 13, 2020 to August 7, 2021. https://www.publichealthontario.ca/-/media/documents/ncov/epi/covid-19-myocarditis-pericarditis-vaccines-epi.pdf?sc_lang=en
214. Polack, F. P. et al. Safety and Efficacy of the BNT162b2 mRNA Covid-19 Vaccine. New England Journal of Medicine 383, 2603–2615 (2020).
215. Krammer F. A correlate of protection for SARS-CoV-2 vaccines is urgently needed. Nat Med 2021 277 [Internet] 2021 [cited 2021 Aug 9];27(7):1147–8. Available from: https://www.nature.com/articles/s41591-021-01432-4
216. Seow J, Graham C, Merrick B, et al. Longitudinal observation and decline of neutralizing antibody responses in the three months following SARS-CoV-2 infection in humans. Nat Microbiol [Internet] 2020;5(12):1598–607. Available from: https://doi.org/10.1038/s41564-020-00813-8
217. Ruopp MD, Strymish J, Dryjowicz-Burek J, Creedon K, Gupta K. Durability of SARS-CoV-2 IgG Antibody Among Residents in a Long-Term Care Community. J Am Med Dir Assoc [Internet] 2021;22(3):510–1. Available from: https://pubmed.ncbi.nlm.nih.gov/33515497
218. Shrotri M, Navaratnam AMD, Nguyen V, et al. Spike-antibody waning after second dose of BNT162b2 or ChAdOx1. Lancet [Internet] 2021 [cited 2021 Jul 22];0(0). Available from: http://www.thelancet.com/article/S0140673621016421/fulltext
219. Israel A, et al. Large-scale study of antibody titer decay following BNT162b2 mRNA vaccine or SARS-CoV-2 infection. medRxiv preprint doi: https://doi.org/10.1101/2021.08.19.21262111;
220. Cho A, et al. Antibody Evolution after SARS-CoV-2 mRNA Vaccination. bioRxiv preprint doi: https://doi.org/10.1101/2021.07.29.454333
221. Neidleman J, et al. mRNA vaccine-induced SARS-CoV-2-specific T cells recognize B.1.1.7 and B.1.351 variants but differ in longevity and homing properties depending on prior infection status. bioRxiv preprint doi: https://doi.org/10.1101/2021.05.12.443888
222. Gazit S, et al. Comparing SARS-CoV-2 natural immunity to vaccine-induced immunity: reinfections versus breakthrough infections. medRxiv preprint doi: https://doi.org/10.1101/2021.08.24.21262415
223. Perez G, Banon T, Gazit S, et al. A 1 to 1000 SARS-CoV-2 reinfection proportion in members of a large healthcare provider in Israel: a preliminary report. medRxiv [Internet] 2021;2021.03.06.21253051. Available from: http://medrxiv.org/content/early/2021/03/08/2021.03.06.21253051.abstract
224. Lumley SF, O’Donnell D, Stoesser NE, et al. Antibody Status and Incidence of SARS-CoV-2 Infection in Health Care Workers. N Engl J Med [Internet] 2021 [cited 2021 Mar 15];384(6):533–40. Available from: http://www.nejm.org/doi/10.1056/NEJMoa2034545
225. Seligmann H. Expert evaluation on adverse effects of the Pfizer-COVID-19 vaccination. https://in-this-together.com/ukc/Selligmann-Yativ-Paper.pdf
226. Israel Ministry of Health: https://datadashboard.health.gov.il/COVID-19/general
227. Israeli Ministry of Health: https://data.gov.il/dataset/covid-19/resource/9b623a64-f7df-4d0c-9f57-09bd99a88880
228. Brown CM, et al. Outbreak of SARS-CoV-2 Infections, Including COVID-19 Vaccine Breakthrough Infections, Associated with Large Public Gatherings — Barnstable County, Massachusetts, July 2021. US Department of Health and Human Services/Centers for Disease Control and Prevention MMWR / August 6, 2021 / Vol. 70 / No. 31.
229. Chau NVV, et al. Transmission of SARS-CoV-2 Delta Variant Among Vaccinated Healthcare Workers, Vietnam. Lancet Preprint. Available at SSRN: https://ssrn.com/abstract=3897733 or http://dx.doi.org/10.2139/ssrn.3897733
230. Elliott J, Whitaker M, Bodinier B, Eales O, Riley S, Ward H, et al. (2021) Predictive symptoms for COVID-19 in the community: REACT-1 study of over 1 million people. PLoS Med 18(9): e1003777. https://doi.org/10.1371/journal.pmed.1003777
231. TWiV 640: Test often, fast turnaround, with Michael Mina. https://youtu.be/kDj4Zyq3yOA
232. Your Coronavirus Test is Positive. Maybe it shouldn’t be. Interview with Michael Mina, MD. Published August 29, 2020; Updated September 17, 2020. https://www.nytimes.com/2020/08/29/health/coronavirus-testing.html
233. Palmer M. Doctors for COVID Ethics Symposium-Session 1: https://www.ukcolumn.org/video/doctors-for-covid-ethics-symposium-session-1-the-false-pandemic
234. Yan L, et al. (2020) Unusual Features of the SARS-CoV-2 Genome Suggesting Sophisticated Laboratory Modification Rather Than Natural Evolution and Delineation of Its Probable Synthetic Route. https://doi.org/10.5281/zenodo.4073131
235. Yan L, et al. https://doi.org/10.5281/zenodo.4028829
236. Comments of Luc Montagnier: https://sharylattkisson.com/2021/06/video-exclusive-investigation-separating-rumor-from-fact-on-covid-19s-origin/
237. Comments of Luc Montagnier: https://luis46pr.wordpress.com/2021/08/19/nobel-prize-winner-urges-public-to-reject-jabs-vaccines-facilitate-development-of-deadlier-covid-variants/
238. New evidence, including a sworn affidavit from Prof. Luc A. Montagnier, has been submitted to the International Criminal Court alleging World Governments are complicit in genocide and crimes against humanity – The Expose. https://theexpose.uk/2021/08/22/new-evidence-submitted-icc-alleging-world-governments-committed-gonocide/
239. Nobel Prize Winner says “Covid Vaccines are an unacceptable mistake” – The Expose. https://theexpose.uk/2021/05/24/nobel-prize-winner-says-covid-vaccines-are-an-unacceptable-mistake/
240. The Origin of the COVID-19: An Investigation of the Wuhan Institute of Virology. House Foreign Affairs Committee Report Minority Staff. https://gop-foreignaffairs.house.gov/wp-content/uploads/2021/08/ORIGINS-OF-COVID-19-REPORT.pdf
241. Professor Mattias Desmet. Why do so many still buy into the narrative? https://odysee.com/@pandemicpodcast:c/compliance:2
242. Professor Mattias Desmet: https://ratical.org/PandemicParallaxView/EyeOfTheStorm-ProfMattiasDesmet.html