Dr. Anthony Fauci has repeatedly emphasized vaccine development to control COVID-19 (Severe Acute Respiratory Syndrome Coronavirus-2 [SARS-Cov2]). His colleague, National Institutes of Health Director Dr. Francis Collins, subsequently interviewed by the Wall Street Journal, provided this caveat: “It would not be particularly encouraging if we have a vaccine that’s capable of protecting 20-year-olds who probably have a pretty low risk anyway of getting sick, and doesn’t work at all for people over 65.” Oxford University vaccine researcher and Regius Professor of Medicine Sir John Bell recently lamented that as COVID-19 cases rapidly dwindle in the U.K.,“You wouldn’t start (trials) in London now for sure.” Bell added that scientists might have to “chase” the virus around the nation for the vaccine trials to be successful.
Vaccine enthusiast Fauci and the more sober Bell each conveniently ignore unsuccessful vaccine experiences with other coronaviruses over the past two decades: (Severe Acute Respiratory Syndrome) SARS-Cov1 and (Middle East Respiratory Syndrome) MERS-Cov. They also seem to have forgotten, amid the COVID-19 hysteria, reassuring, almost 100-year-old basic concepts of naturally acquired community immunization, made clear prior to modern-era mass vaccination campaigns.
Since their emergence in 2003 and 2012 respectively, no safe and efficacious human vaccines for either SARS-Cov1 or MERS have been developed. Moreover, experimental non-human (animal model) evaluations of four SARS-Cov1 candidate vaccine types, revealed that despite conferring some protection against infection with SARS-Cov1, each also caused serious lung injury, caused by an overreaction of the immune system, upon viral challenge. Identical “hypersensitive-type” lung injury occurred when mice were administered a candidate MERS-Cov vaccine, then challenged with infectious virus, negating the ostensible benefit achieved by their development of promising so-called “antibodies” (produced by a class of cells that can circulate in blood called “B-cells”), which might have provided immunity to MERS-Cov.
These disappointing experimental observations must serve as a cautionary tale for SARS-Cov2 vaccination programs to control epidemic COVID-19 disease.
Absent tenable vaccination programs, what alternative strategy might be deployed to blunt the advance of COVID-19? It is the same goal as of a successful vaccine — achieving “herd immunity.”
Although the term “herd immunity” was first coined in 1923, it only became broadly used, stimulated by increased vaccine use over the past five decades, when discussing disease eradication. Contrary to the vaccination paradigm of “eradicating” disease, herd immunity, including its mathematical underpinnings (a 1927 theorem still applied by vaccine modelers), was originally conceptualized to address this question:
Assuming a given total quantity of resistance against a specific (bacterial) parasite to be available among a considerable population, in what way should that resistance be distributed among the individuals at risk, so as best to ensure against the epidemic spread of the disease, of which the parasite is the causal agent?
These original conceptions further acknowledged the influence of differences in disease susceptibility upon herd immunity: “The resistance of the herd at any given moment will be determined by the frequency (distribution) within it of individuals of varying orders of susceptibility.”
Even the foundational modelers, whose seminal 1927 paper was “limited to the case in which all members of a community are initially equally susceptible to the disease” — an assumption still used by vaccine-driven disease eradication or near-eradication modeling — emphasized:
The epidemic continues to increase so long as the density of the unaffected population is greater than the threshold density [the threshold of “herd immunity” or “herd immunity threshold”], but when this critical point is approximately reached the epidemic begins to wane, and ultimately to die out. This point may be reached when only a small proportion of the susceptible members of the community have been affected.
An important added observation (from 1929) extended the concept of herd immunity beyond prevention of symptomatic infection to include protection against non-fatal and certainly less morbid illness: “This immunity may be acquired latently, without illness, and, even if not always enough to prevent symptomatic infection, may be such that severity and fatality are decreased.”
Classic theory based on the assumption of “homogeneity,” specifically equal susceptibility to disease, is still invoked when estimating the herd immunity threshold (HIT) required for disease eradication or near-eradication by mass vaccination. The HIT, the proportion of immunity (p) within a given population beyond which the effective reproduction number (R0) of an infection is one — i.e. when each infected person transmits the infection, on average, to just one other person — is given by the equation p=HIT= (R0-1/ R0).This is an oversimplified model of a homogeneous population in which an infected individual is equally likely to infect R0 other individuals, all of whom are susceptible hosts at the outset, while it is further assumed that the entire population has the same R0 value. Such oversimplified HIT calculation methodology, and the goal of disease-eradication/near-eradication, now frames the discussion of herd immunity against COVID-19. Calculations based upon these assumptions predict the HIT “must exceed 0.67” before the incidence of SARS-CoV2 infection will start to decline.
Several investigators, however, have challenged the validity of reflexively applying this vaccine-based paradigm — specifically the assumptions of homogeneity, but also, at least indirectly, the corollary goal of COVID-19 eradication/near-eradication. Acknowledging the self-evident variability of both susceptibility and R0, “spread-ability,” within populations, they have re-calculated HITs for COVID-19 considerably below the allegedly “axiomatic” cutpoint of “> 0.67.” Their sound modeling methods capture real-world, commonsense host-disease interaction heterogeneity. They argue that R0 must vary, since some people are more likely than others to transmit infection due to occupation, environment, lifestyle, and other factors. For instance, an infected, married health care worker with a family (and perhaps extended family) has a much greater potential to infect others compared to a single person working alone from home. In practice, both R0 and host susceptibility are variable, and this variation can profoundly lower HITs.
Thus a respected team of infectious disease epidemiologists from the U.K. and U.S. have concluded: “Naturally acquired immunity to SARS-CoV-2 may place populations over the herd immunity threshold once as few as 10-20% of its individuals are immune.” Separate calculations of HITs ranging from ~18% to 43% — each substantially below the dogmatically asserted value of ~70% — have recently been reported.
Additional immune responses beyond the development of specific SARS-Cov2 “B-cell antibodies,” capable of lowering the HIT by preventing SARS-Cov2 infection and/or reducing COVID-19 disease severity, have been described. These include:
The Centers for Diseases Control and Prevention (CDC) published a 5/20/20 “best estimate” of the infection fatality ratio (IFR) for COVID-19 in the U.S. An IFR for any infectious disease is the number of fatal infections divided by the total of all infections, including asymptomatic infections. The CDC’s COVID-19 IFR for the U.S. ranged from 0.20%-0.27%, based upon asymptomatic infections composing an estimated 50% to 35% of total infections. This CDC estimate is consistent with its calculation of a 0.26% U.S. IFR for the 1957-58 H2N2 influenza A pandemic, despite an attempted vaccination program. Stanford Professor of Epidemiology John Ioannidis’ 5/19/20 analysis of COVID-19 IFRs from 12 large population studies that surveyed the presence of COVID-19 antibodies in blood, each with at least 500 sampled, found: 7/12 with a corrected IFR range of 0.06%-0.16%, like seasonal flu; 3/12 modestly higher, 0.25%-0.40%; and 2/12 modestly lower, 0.02%-0.03%.
COVID-19 summary IFRs in these much less than calamitous ranges should raise more questions, beyond unproven safety and efficacy, about the urgency of vaccine development, and certainly mass deployment. Independent confirmation of these IFR estimates was provided by the world’s most populous nation, India. As reported in early June, the Indian Council of Medical Research “has now estimated that the fatality rate due to the infection is very low at 0.08%.” The relatively benign nature of COVID-19 in children, compared to seasonal influenza, should further give us pause. For example, using mortality data available through May 8, 2020, U.S. children 0-14 years old were ~7 times more likely to die from influenza this year, despite vaccination programs, than from COVID-19.
Naturally acquired herd immunity to COVID-19 combined with earnest protection of the vulnerable elderly — especially nursing home and assisted living facility residents — is an eminently reasonable and practical alternative to the dubious panacea of mass compulsory vaccination against the virus. This strategy was successfully implemented in Malmo, Sweden, which had few COVID-19 deaths by assiduously protecting its elder care homes, while “schools remained open, residents carried on drinking in bars and cafes, and the doors of hairdressers and gyms were open throughout.”