The WSJ Perspective

Allysia Finley, a journalist for the WSJ, referenced a study published in Nature that examined the evolution of Omicron. The study concluded that immune imprinting from vaccines could have influenced the emergence of XBB. This research explored the immune evasion abilities and mutation profiles of various Omicron variants, revealing that XBB and BQ1.1 demonstrated significant resistance to both monoclonal antibodies and antibodies from vaccinated individuals, while maintaining their ability to bind to cells. This resistance was notably comparable to the original SARS-CoV-1 from 2002/2003, indicating a significant evolutionary leap.

The study also traced how XBB evolved, finding signs of immune imprinting as early as the BA.2 and BA.5 vaccine breakthrough cases, where antibodies predominantly targeted the original Wuhan strain. In contrast, Omicron-specific antibodies were infrequently found in vaccinated individuals, unlike in those who were unvaccinated and contracted Omicron.

Immune imprinting occurs when older antibodies, generated from previous variants, continue to respond to newer variants. This can hinder the development of effective new antibodies. Immune imprinting has been observed in responses to both the influenza vaccine and the human papillomavirus vaccine.

Further analysis revealed that non-Omicron-specific antibodies imposed immune pressure, favoring the survival of Omicron variants while eliminating non-Omicron mutations. This phenomenon helps to explain why Omicron remains the dominant variant today, as vaccine-induced immunity has effectively removed non-Omicron variants.

Finley cited additional studies indicating that vaccine-induced antibodies were significantly weaker against the XBB variant compared to the original Wuhan variant.

Next, Finley referred to the controversial Cleveland Clinic study, which suggested a higher rate of infection among those who received more vaccines. While this finding may seem alarming, it's essential to consider the context. Although some studies indicate that vaccinated individuals are experiencing more Omicron infections, the risk of severe illness remains lower with increased vaccination.

Several factors could explain this discrepancy, including behavioral differences (e.g., vaccinated individuals are often in higher-risk situations), IgG4 class switching, and immune imprinting.

Finley also noted that initial surges of XBB occurred in regions with high vaccination and boosting rates, such as Singapore and the Northeast U.S. Conversely, XBB spread more slowly in areas with lower vaccination rates, like the South and Midwest U.S.

Finley concluded by asserting that while vaccines initially reduced severe illness, experts are hesitant to acknowledge that boosters may be yielding diminishing returns and could even increase vulnerability to new variants like XBB.

The Essence of Finley's Argument

Finley's main point is that immune imprinting from vaccines creates selection pressure that eradicates older variants, favoring the emergence of newer variants. This selection could explain why XBB and similar Omicron variants have surged even in highly vaccinated regions.

Her argument aligns with the controversial "leaky vaccine" hypothesis promoted by Geert Vanden Bossche, Ph.D. In essence, because Covid-19 vaccines are designed to reduce severe disease rather than prevent infection and transmission, they may inadvertently promote the survival of more transmissible variants. While this perspective has some merit, Bossche has also made other questionable claims that have been addressed by experts.

Alternative Expert Opinions

Kristen Panthagani, MD, Ph.D., a resident at Yale New Haven Hospital, emphasized that variants arise from infections rather than vaccinations. She pointed out that vaccines don’t function like antibiotics, which can be easily overcome by resistant strains. Instead, vaccines train the immune system as a whole, making the evolution of vaccine resistance unlikely.

Nevertheless, variants like Omicron can emerge that evade prior immunity. Panthagani explained that if a new variant develops the ability to partially escape vaccine-induced immunity, it will spread more readily. However, this does not imply that vaccinated individuals increase the likelihood of vaccine-resistant variants arising.

Journalists Faye Flam and Jesse Bloom provided counterarguments to the WSJ piece. Flam pointed out that XBB.1.5 did not originate in areas with high vaccination rates; instead, it likely emerged in Asia, where vaccination rates are also high.

Flam acknowledged that while vaccines do exert evolutionary pressure on the virus, suggesting they worsen the situation is misleading. Without vaccines, the spread of immune-evading variants would still occur, likely resulting in more fatalities.

Evaluating the WSJ Hypothesis

In summary, the WSJ hypothesis holds some truth, though interpretations vary. Darwinian evolution relies on random mutations and natural selection. Genetic mutations occur randomly, which may enhance or diminish an organism's ability to survive. Nature, including vaccination, then selects for advantageous mutations.

From the perspective of random mutations, vaccines are not responsible for the emergence of Omicron variants. However, vaccines do impose selection pressure that allows vaccine-resistant variants to survive. Thus, while vaccines may contribute to the selection of these variants, it would be unfair to solely blame them, as natural immunity also exerts similar pressures.

Historically, vaccines have occasionally led to the evolution of immune-evasive traits in some pathogens. For instance, the emergence of vaccine escape mutants in pneumococcus after the widespread use of the 7-valent pneumococcal conjugate vaccine (PCV7) exemplifies this.

Ultimately, vaccines are just one of our tools in combating pathogens, and pathogens can adapt in response. The ongoing evolutionary arms race complicates the assignment of blame, as each factor plays a role to varying degrees.

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