by James Lyons-Weiler, PhD, Popular Rationalism, ©2024
(Oct. 17, 2024) — The hype surrounding mRNA vaccines, hailed as groundbreaking, has masked a critical reality: the natural evolutionary dynamics of RNA viruses and the nature of the vaccines themselves will inherently limit their effectiveness in the long term. This was clear before 2020.
Significant biological concerns regarding mRNA vaccines themselves are emerging. Biodistribution studies have shown that the lipid nanoparticles (LNPs) used to deliver mRNA spread throughout the body, accumulating in organs like the liver, spleen, and ovaries—far beyond the intended injection site. This raises questions about long-term safety, particularly as evidence mounts of LNP toxicity in various tissues.
Laboratory evidence suggests that genotoxicity is a real risk. mRNA can potentially integrate into the human genome in the presence of reverse transcriptases, which are naturally present in the body. This concern is not limited to the mRNA in the jabs but extends to any DNA or RNA contaminants that may be introduced during manufacturing, posing additional risks.
Multiple Selection Types and Targets Thwart Lasting Protective Immunity from mRNA Vaccines
Vaccine-Induced Selection Pressure: The use of vaccines, especially those targeting only specific viral epitopes like the spike protein in SARS-CoV-2, focus the immune system on those targeted regions. This creates strong selection pressure on the virus to evolve variants that can evade the immune response trained by the vaccine. This process called vaccine-induced immune escape, can lead to variants with mutations in the spike protein that reduce vaccine efficacy, which is why variants like Delta or Omicron emerged with mutations specifically in the spike protein.
One dangerous consequence of this narrow immune focus is the potential development of Antibody-Dependent Enhancement (ADE). ADE occurs when antibodies produced by vaccination or prior infection, instead of neutralizing the virus, enhance its entry into host cells, leading to more severe infections. This phenomenon arises when the virus mutates so that vaccine-generated antibodies bind to it but fail to neutralize it, facilitating its entry into cells.
Vaccine-induced selection pressures can accelerate this risk by pushing the virus to evolve variants that partially escape immune surveillance. The immune system may recognize these escape variants but not thoroughly neutralize them, providing the perfect conditions for ADE. Thus, viral evolution driven by vaccines could lead to an increase in pathogenicity rather than a reduction, especially in populations where the vaccine induces intense but narrowly targeted immune responses.
Vaccines designed against a narrow set of epitopes can inadvertently accelerate the evolution of escape variants, as the virus needs only to mutate in specific regions to evade the trained immune response. Evolutionary biologists have long been aware of this risk in pathogen evolution, mainly when dealing with RNA viruses, whose rapid replication and error-prone polymerases provide a high mutation rate.
Natural Infection-Induced Selection Pressure: Unlike vaccine-induced immunity, natural infection exposes the immune system to a broader range of viral epitopes, including those outside the spike protein. This broader exposure generally reduces the chances of immune escape because the virus would have to mutate simultaneously across multiple regions of its genome to evade natural immunity. However, natural immunity still exerts selection pressure, particularly on epitopes recognized and targeted by the immune system. The virus may evolve to avoid these natural immune responses, leading to changes in viral genome regions previously targeted by the host’s immune defenses.
PCR Testing-Induced Selection Pressure: The widespread use of PCR testing, which relies on detecting specific viral sequences, inadvertently creates a unique selection form. PCR tests use primers complementary to specific regions of the viral genome, and if mutations arise in those regions, the virus could evade detection. Over time, this selects viral variants that no longer match the primer sequences used in PCR tests, thus escaping detection. This scenario creates an artificial selection pressure on the virus at the genomic level, favoring variants that either mutate away from the tested regions or reduce their expression, enabling the virus to spread undetected.
We saw this in the UK with the infamous S-gene drop out, in which a PCR diagnostic test primer location on the spike protein coding region evolved away from a primer match to prevent that primer pair from reporting the presence of the virus when it was, in fact, present. Andrew Rambaut was evidently unaware of the problem that in a 2/3 diagnostic rule, one dropping out would reduce senstivity to by 50%. I pointed this out to him by email after he had published that the S-gene drop-out was potentially a useful way to differentiate among variants (not true). The S-gene drop-out occured 8 months before it was detected, meaning that people in the UK testing negative had approximately a 50% chance of a negative PCR result if they had the S-gene dropout variant, believing themselves to be free of the virus. (NB: I am not arguing for the use of PCR testing for mRNA viruses; I am simply sharing facts).
Vaccine-Induced Selection via Iatrogenic Illness: Vaccine-induced iatrogenic illness introduces an additional selection pressure on viral evolution, but only if the epitopes responsible for the adverse reactions are also present in circulating viral variants.
Moreover, iatrogenic autoimmune effects could create new evolutionary pressures on both the immune system and the virus. If specific individuals develop autoimmune responses due to molecular mimicry between viral and their private human epitopes (as seen with the Titan protein homology (found first by Lyons-Weiler, studied intensively by Kanduc)), this creates a dual challenge. The virus faces selective pressure to evade vaccine-induced immunity and may also evolve to exploit populations experiencing vaccine-induced immune dysregulation. This could encourage the emergence of variants that target the immune-compromised individuals more effectively, maintaining transmission despite increased immune activity. The vaccines are known now to produce many other conditions, including cardiovascular (myocarditis and pericarditis), menstrual irregularities, blood clotting disorders, neurological symptoms, autoimmune disorders, and dysautonomia. This interaction between iatrogenic illness and viral evolution requires careful study, as the long-term impacts of chronic illness have numerous potential inputs and responses induced by vaccines, each of which may reshape how viral populations evolve within the human host – and the human host evolution as well.
Autoimmunity via Pathogenic Priming
When a vaccine targets specific epitopes and induces harmful autoimmune responses (iatrogenic illness) in some individuals, these epitopes become selection factors that could influence viral evolution. Suppose the circulating virus contains the same epitopes causing autoimmune reactions. In that case, the virus faces selective pressure to evolve variants that modify or evade these epitopes to survive in the vaccinated population. Over time, this dynamic could favor the spread of variants with altered epitopes, thus shaping the viral population in response to vaccine-induced immunity and the potential for iatrogenic effects. However, this evolutionary pressure is only relevant when the viral and vaccine epitopes overlap significantly.
Each of these mechanisms represents an evolutionary pressure that pushes the virus to adapt and evolve in ways that thwart public health control measures. In some ways, these pressures act synergistically, each focusing on different aspects of the viral genome or life cycle, potentially accelerating the virus’s evolutionary rate. In other ways, selection could counterbalance (negative selection on specific mutations on the PCR primer binding site could counterbalance selection of those mutations given their contribution to viral fitness for virulence or transmission.
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