Herd Immunity and Other Viral Infections
Parts 1 & 2 might lead someone to wonder how herd immunity can operate for other infectious diseases. Measles, polio, and smallpox are viral infections for which vaccines have allowed the development of herd immunity (and eradication in the case of smallpox).1 These viruses replicate only in humans. Additionally their infections or vaccinations confer lasting, solid immunity, often for the lifetime of an individual.
Bottom line: All three conditions required for herd immunity are met with regard to measles, polio, and smallpox viruses.
LIE 3: Ignoring the variant-generating potential of SARS-CoV-2
It is worth discussing other ways that SARS-CoV-2 differs from these viruses. SARS-CoV-2 is a single-stranded RNA virus.2 It is well-established that RNA viruses generally have higher mutation rates than DNA viruses (such as smallpox). Having a high mutation rate means that changes to the genetic material occur very commonly and may accumulate in ways that affect components of a virus. When these changes occur, they have three general options: help the virus; hurt the virus; or not have much effect for virus survival. Just by the nature of probabilities, a virus that has a higher mutation rate coupled with the vast amount of replication that occurs in just a single infection means that mutations which allow for evasion of immunity may more commonly arise in viruses such as these. Take this together with the massive global scale of case numbers in only a few months and the scene was set from the beginning for variants to emerge. The sheer magnitude of cases is owed to the highly transmissible and infectious nature of SARS-CoV-2 (infecting human cells more easily, possible spread during the prodromal phase, a reproductive number, R0, >1).3 4
Coronavirus mutation rates are estimated as moderate to high when compared with other single-stranded RNA viruses.5 A few early 2020 studies suggested that SARS-CoV-2 mutation rate may be lower than usual for RNA viruses.6 7 However, other studies,8 9 10 11 12 13 especially by mid-2020 and beyond, reported the opposite conclusion. Interestingly, a similar kind of trend occurred regarding the original SARS outbreak. During the global SARS outbreak, studies conducted earlier, or using earlier data, reported relatively low mutation rates or “slow evolution” as compared to other RNA viruses14 15, but later studies reported mutation rates similar to RNA viruses.16 17 18 (22) Proposed reasons for these differences were that early studies may have assessed “an early stage of the virus evolution”19 compared with a “broader sample collection over a longer period of time”20 for later studies and recognizing that the adaptive process can take years.21 This relates to what’s known as the “phylodynamic threshold”- whether a virus has had sufficient time to evolve since its origin (8). One review paper from 2012 states that “SARS-CoV genomes evolved rapidly in marketplace animals, suggesting that the virus was still adapting to these animals rather than persisting in equilibrium, as would be expected in a reservoir species.”22
Even if early in the COVID-19 pandemic some research raised the possibility of slower than usual evolutionary rate, prior SARS analyses combined with the growing consensus in the literature that SARS-CoV-2 was acquiring mutations at a rate similar to other RNA viruses warranted acknowledgement that its variant-generating potential could have important implications. Likely progression to endemic status (more similar to the flu) and capability to evade prior immunity, making the publicly touted protocol for vaccines naive and unrealistic (more on this later), are two huge probabilities kept from the public for more than a year and a half. In fact, “fitness-enhancing mutations were first detected to have arisen within a few months of the evolution of SARS-CoV-2 within the human population (25).” Indeed, it was clear by November of 2020 that variant emergence was significantly increasing.23
Just to clarify, the term “variant” merely refers to genomes that differ in sequence, with as little as one unique mutation, whereas a “strain” refers to a variant with phenotypic change(s) that can allow for differences in antigenicity, transmissibility, or virulence.24 Hundreds of variants were already present in populations by early 2020 (example: 160 genotypes with 10 central variants in the below figure), and nearly 200,000 by the end of 2020.25 By early 2021 a study analyzed over 1 million unique genotypes!26 If this comes as a shock, it’s probably because we were led to think (if it were even mentioned) only a handful had arisen.
This quote from an April 2019 article27 regarding SARS-CoV and MERS-CoV seems apropos:
“…coronaviruses may have the potential to cause devastating pandemics due to unique features in virus biology including rapid viral replication, broad host range, cross-species transmission, person-to-person transmission, and lack of herd immunity in human populations.” <emphasis added>
They also go on to say that biological factors increasing cross-species or person-to-person spread (which of course has occurred for SARS-CoV-2) may make timely quarantine ineffective to contain spread.
From a SARS-CoV 2004 article (10), another quote to bake your noodle:
“If the pathogen evolves slowly, there will be a better chance for development of effective long lasting vaccines and successful treatment for patients from a particular geographic region will likely be effective for patients from other areas. On the other hand, if the pathogen (particularly the genes coding for major antigens) evolves rapidly, an effective strategy to prevent transmission of the SARS-CoV must be the top-priority, and an effective vaccine program may be problematic.”
From a different SARS-CoV 2003 article:
“…the genetic mutability of SARS-CoV, especially in the segments encoding the major antigenic proteins, would also have an effect on development of broadly effective vaccines.”
That statements such as these were available throughout the peer-reviewed literature, far before COVID-19 was even a twinkle in Fauci’s eye, should raise some eyebrows. Or even stir up some ire.
Bottom line: By its nature, SARS-CoV-2 is and always was likely poised to be capable of generating an immense amount of variants, more similar to the common cold or flu. Yet somehow when considering our path forward through the pandemic, this was largely ignored. Again, how can such a discrepancy accidentally occur in the minds of our guiding “experts”?
LIE 4: Ignoring evolutionary stability: comparing smallpox, poliovirus, or measles to SARS-CoV-2
Contrast this with smallpox, poliovirus, or measles. In general these viruses are all relatively evolutionarily stable.
Smallpox is a DNA virus, which as mentioned yields a lower intrinsic mutation rate. This contributed to the durable immunity produced after either infection or vaccination.28 With less mutation and less successful variant production, a given vaccine or natural infection can confer immunity that will more likely succeed in the longterm.
Despite measles being an RNA virus, the measles vaccine still confers durable immunity to all circulating variants, even though it is based on a lab-adapted isolate from the throat of David Edmonston in 1954! A recent paper29 demonstrated that its evolution is constrained by several mechanisms, which make an accidental emergence of a variant capable of evading this immunity very statistically improbable, in fact “near-zero.” They contrasted this with other respiratory RNA viruses, like influenza or coronaviruses, which require relatively few single substitutions to achieve evolutionary advantage.
Poliovirus is another RNA virus, however, there are only three known wild-type strains, despite it first being identified in 1894 in the U.S.30 For over 125 years, there are only three strains! Regardless of the mechanism(s) by which this occurs (indeed, a characterization of which has not yet been identified as of a Jan. 2020 publication), it signifies that poliovirus is evolutionarily stable.
Bottom line: SARS-CoV-2 by its nature, is not (and never was) comparable to smallpox, poliovirus, or measles virus with regard to respective viral properties and the likelihood of developing durable immunity to all future variants, whether vaccine-induced or naturally-acquired.
Success of vaccines for these other viruses has been possible largely due to the evolutionary stability of these viruses, which allows for the possibility of solid, durable immunity (further discussion later). Much like the common cold or influenza, SARS-CoV-2 mutation is going to occur, which at some point might make any prior immunity possibly imperfect or even obsolete. SARS-CoV-2 is not comparable to smallpox, measles, and poliovirus. So again, what place did this lie have in the COVID-19 narrative? Why another deception to the public?
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