Worse than We Thought: Pathogenic Priming Likely Far More Widespread Due to Pseudouridine in Altered Spike mRNA Injections

Rogue proteins not intended from spike mRNA are candidates for molecular mimicry.

The novel mRNA vaccine technology given emergency use authorization is now known to be fraught with risks – some of which were foretold before the production of specific mRNA injectables. These vaccines, which include those developed by Moderna and Pfizer-BioNTech, are supposed to work by delivering genetic instructions to our cells, instructing them to produce a piece of the virus known as the spike protein. This, in turn, triggers an immune response, preparing the body to fight the real virus if it later enters the body. One of the first peer-reviewed studies to alert to the problem of using spike protein was my own, published in April 2020, in which I introduced the concept, now known as pathogenic priming.

The process of pathogenic priming refers to the possibility that exposure to a vaccine could, in some cases, enhance the disease in the vaccinated upon subsequent repeated exposures to the same offending epitopes via infection – or follow-up injection. The process has raised concerns within the scientific community: it has been challenged and validated in the lab, and it has been cited hundreds of times.

One specific aspect of mRNA vaccine technology that could potentially contribute to pathogenic priming is the use of pseudouridine, a synthetic modification introduced to increase the stability of the mRNA and its acceptance by the human immune system.

Recent research has highlighted a fatal flaw in mRNA technology that impairs the process of protein translation process from mRNA within human cells. This problem involves a well-known issue of frameshifting, where the reading frame of the mRNA is altered due to slippage of the translational machinery on the pseudouridine, resulting in the production of unintended and abnormal proteins, colloquially referred to as “rogue proteins.”

These rogue proteins themselves represent a population of proteins with additional opportunities for happenstance matches in 3D to human proteins, thus training and confusing antibodies to attack human tissues via self-reactive antibodies. Thus, mRNA vaccine-related pathogenic priming is likely far worse than originally anticipated, as the number and types of epitopes the immune system will train to have nothing to do with SARS-CoV-2 immunity – leading to major off-target deviations from the intended immune response elicited by the vaccine.

This article aims to explore the intricate relationship between pseudouridine-induced frameshifting and the production of rogue proteins in the context of mRNA vaccines. By focusing on the scientific evidence surrounding frameshifting, the nature of the rogue proteins produced, and their potential implications for vaccine safety and efficacy, we seek to provide a comprehensive understanding of this critical issue. As we navigate the complexities of mRNA vaccine technology, it is essential to balance the immense benefits these vaccines offer in controlling infectious diseases with the ongoing need to ensure their safety for all individuals.

Understanding mRNA Vaccines and Pseudouridine

mRNA vaccines represent an entirely novel approach in public health’s attempts to fight against infectious diseases. They are supposed to use our body’s cellular machinery to produce a viral antigen, which is then supposed to stimulate a precise immune response. This method contrasts traditional vaccines, which often use weakened or inactivated forms of a virus. The heart of mRNA vaccine technology lies in its use of messenger RNA (mRNA) strands, which carry the genetic instructions for cells to produce the virus’s spike protein, mimicking an infection and prompting the immune system to respond.

Both Pfizer and Moderna chose to use pseudouridine to replace uridine, one of the four standard nucleosides in RNA, ostensibly to evade the body’s innate immune response to foreign RNA. This modification allows the mRNA strand to enter cells and produce the viral protein without being prematurely destroyed by the body’s defenses.