Friday, 18 April 2025

Vaccine vs. Wild Measles: No Peer-Reviewed Proof of Reduced Spread or Replication


Vaccine vs. Wild Measles: No Peer-Reviewed Proof of Reduced Spread or Replication

Faith in vaccines isn’t science—zero direct evidence shows the virus in the measles vaccine isn’t more infectious or doesn’t replicate more in human patients than the wild virus

This post was published by Jon Fleetwood. Please visit his Substack and subscribe to support his work. Follow Jon: Instagram @realjonfleetwood / Twitter @JonMFleetwood / Facebook @realjonfleetwood

Editor’s Note: I’ve run this article through four different artificial intelligence (AI) systems, asking them whether anything I’ve written in this article is false. ChatGPT, Twitter/X’s Grok, Google’s Gemini, and Perplexity all confirm everything below is accurate. Try it yourself: Paste my headline into one of these AIs. Read the response. Then paste the body of my article. Read the response. Ask it if the information is accurate. I’ve provided the responses that all four AIs gave to this question underneath this article’s conclusion.

Despite decades of widespread use and confidence in the measles vaccine, there is a striking gap in the scientific literature: no peer-reviewed studies directly confirm that the vaccine-type measles virus (Edmonston strain) is less infectious or replicates less than the wild-type measles virus (Montefiore strain) in human patients.

This fact raises important questions about assumptions underlying vaccine development and deployment. Without direct evidence, we are left to rely on assumptions rather than definitive proof, which could have serious implications for understanding how the vaccine strain behaves in human populations.

This also raises the possibility that the vaccine-type virus could, in fact, be more infectious and replicate more efficiently than the wild-type virus in certain contexts.

Only Indirect Evidence Suggests Attenuation

Existing studies rely on indirect evidence from laboratory experiments, animal models, and epidemiological observations to suggest that the vaccine strain has attenuated replication. For example:

  • Animal Studies: Research in rhesus macaques shows that wild-type measles virus replicates efficiently in lymphoid tissues, spreading systemically and persisting for weeks. In contrast, the vaccine strain primarily replicates in respiratory tissues and is cleared more quickly.
  • Implication: While this suggests reduced replication in animals, it does not prove that the same reduction occurs in humans. Without direct human studies, we cannot be certain that the vaccine strain behaves as intended across all tissues in real-world conditions. This leaves open the possibility that the vaccine strain could replicate more efficiently than expected in certain human tissues.
  • In Vitro Studies: Laboratory experiments indicate that vaccine strains infect human endothelial cells and dendritic cells more efficiently than wild-type strains but produce less infectious virus overall.
  • Implication: The ability of the vaccine strain to infect a broader range of cells (via CD46) raises concerns about whether it could theoretically infect more tissues or spread differently in humans, even if replication efficiency is lower. This creates uncertainty about its behavior outside controlled laboratory settings and raises questions about whether it could lead to greater infectivity under specific conditions.
  • Gain-of-Function Modifications

    The vaccine strain’s ability to bind CD46—a receptor expressed on all nucleated human cells—represents a clear gain-of-function (GOF) adaptation. This receptor shift occurred during tissue culture passaging, enabling the vaccine virus to infect a broader range of cell types compared to the wild-type virus, which primarily targets immune cells via CD150.

  • GOF research raises concerns about whether broader receptor usage could theoretically enhance infectivity or replication under certain conditions.
  • Implication: The fact that the vaccine strain gained a new ability to infect more types of cells is significant—this functional expansion could lead to unintended consequences such as increased infectivity or unexpected tissue tropism. Without direct human studies, we cannot rule out these possibilities.
  • Despite this functional expansion, claims of attenuation remain unconfirmed by direct human studies.
  • Implication: The idea that attenuation offsets these concerns is based on indirect evidence rather than definitive proof from human patients. This leaves room for doubt about whether attenuation fully mitigates risks associated with GOF modifications—and whether these modifications might actually make the vaccine strain more infectious or capable of replicating more efficiently under certain circumstances.
  • Texas Measles Outbreak Raises Questions About Vaccine Design

    The ongoing measles outbreak in Texas adds urgency to these unresolved questions about vaccine strain behavior. Texas administered 15,000 more MMR doses this year compared to 2024, yet measles cases have surged beyond last year’s nationwide total. As of late March 2025:

  • 309 Cases Reported: Texas has recorded 309 cases since January—more than the entire U.S. total for 2024 (285 cases).
  • Growing Spread: Measles cases are still rising rapidly across West Texas, with local health officials warning that case numbers are likely undercounted and will continue climbing for months.
  • This paradox—more vaccinations coinciding with more measles cases—raises troubling questions about whether factors related to vaccination campaigns could inadvertently contribute to outbreaks:

  • Vaccine Shedding: Studies confirm that the live measles vaccine virus can shed for up to 29 days post-vaccination, potentially exposing unvaccinated individuals to the attenuated virus.
  • GOF Concerns: The engineered ability of the vaccine virus to bind CD46 could theoretically allow it to infect a broader range of human cells compared to wild-type strains.
  • While most cases involve unvaccinated individuals or those with unknown vaccination status, this outbreak highlights gaps in understanding how vaccination campaigns interact with population dynamics and viral behavior.

    Gaps in Research

    No peer-reviewed studies have directly compared infection rates or replication efficiency between vaccine-type and wild-type measles viruses in humans. Key unanswered questions include:

  • Does the vaccine strain infect fewer cells or replicate less efficiently than the wild-type virus in human tissues?
  • Implication: Without this data, we cannot conclusively say that the vaccine strain behaves as intended or poses no risk of increased infectivity compared to the wild-type virus. This leaves open an alarming possibility: Could the vaccine strain actually replicate more effectively under certain conditions?
  • Could broader receptor tropism (via CD46) lead to unexpected behaviors or increased infectivity?
  • Implication: The ability of the vaccine strain to bind CD46 means it has access to almost all nucleated human cells—a much larger range than wild-type strains targeting immune cells via CD150. This raises concerns about potential tissue-specific effects or behaviors that have not been studied and whether this expanded tropism might increase its ability to spread.
  • Implications for Public Health

    While decades of epidemiological data purportedly support the safety and efficacy of measles vaccines, this gap highlights the need for further research to address unresolved questions about vaccine strain behavior. Ethical constraints make direct human trials challenging, but advancements in modeling and genomic analysis could provide insights into these mechanisms.

  • Implication: Public health decisions rely on robust scientific evidence, yet this gap reveals an area where assumptions are being made without direct validation. Transparency and further investigation are essential to ensure confidence in vaccination programs—and to rule out any potential risks that might arise from GOF adaptations.
  • Conclusion

    The absence of direct studies confirming reduced infectivity or replication of the measles vaccine virus compared to the wild-type virus underscores a significant gap in scientific understanding. This fact does not diminish the proven benefits of vaccination but calls for greater transparency and rigorous investigation into assumptions underlying vaccine design. 

    Without addressing these gaps, we risk overlooking critical aspects of how engineered viruses behave in humans—an oversight that could have far-reaching consequences for public health and scientific integrity.

    Furthermore, it raises an unsettling question: Could the vaccine-type measles virus actually be more infectious or replicate more efficiently than its wild-type counterpart?

    Until direct studies are conducted, this possibility cannot be definitively ruled out—and recent outbreaks like Texas’s record-breaking surge demand urgent answers about how vaccination campaigns interact with viral dynamics and population immunity.

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