Exploring Links Between Prion Diseases and COVID-19 Vaccines
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Understanding Prion Diseases
Prion diseases, often referred to as transmissible spongiform encephalopathies (TSEs), represent a rare and fatal category of neurodegenerative disorders. These diseases are among the deadliest known to humanity, with survival rates approaching zero. Approximately 85% of individuals diagnosed with a prion disease succumb within the first year after symptoms appear. Prion diseases are uniquely lethal because prions, the infectious agents involved, evade detection by the immune system, leading to irreversible neuronal damage and death within a few years.
Prions are not like conventional pathogens; they are simply infectious proteins that can transmit disease, primarily through contact with infected meat or brain tissue, often in cases of cannibalism. Despite their severe impact, prion diseases are exceedingly rare, affecting roughly one in a million people annually, with about 5–15% of cases having a genetic basis.
So, where do COVID-19 and its vaccines fit into the picture of prion diseases?
Theoretical Connections Between COVID-19 and Prion Diseases
An extensive review of scientific literature reveals that most research attempting to connect COVID-19 with prion diseases is largely theoretical. At least six review articles have been published discussing how COVID-19 might trigger or exacerbate prion diseases. Here are three significant observations from this body of work:
- The S1 subunit of the SARS-CoV-2 spike protein features domains that resemble prions and may aggregate with other proteins, potentially leading to prion diseases. However, it's essential to note that the function of a protein is determined by its overall structure, not just individual domains. A study subsequently indicated that these prion-like domains interact with the ACE2 receptor on cell surfaces, suggesting they are unlikely to form harmful aggregates unless they exist independently or dominate the protein's structure. Notably, numerous human proteins also contain prion-like domains without resulting in prion diseases.
- A bioinformatics study suggested that the SARS-CoV-2 spike protein binds strongly to heparin domains in other proteins, including prion proteins. However, this modeling approach has significant limitations, as findings from computational models don't always reflect biological realities. Furthermore, the model used generalized prion protein structures, which can vary greatly in terms of their properties and effects.
- Inflammatory responses associated with COVID-19 are linked to specific microRNAs (miRNAs), including NF-kB (p50/p65)-sensitive miRNA-146a-5p, which is also implicated in prion diseases. While inflammation can aggravate various conditions, it is not sufficient to draw direct links between COVID-19 and prion diseases. For instance, both COVID-19 and AIDS impact CD4 T-helper cells, but this does not imply that COVID-19 contributes to the onset of AIDS. Additionally, miRNA-146a-5p is associated with a wide array of viral and neurological disorders.
Moreover, surveillance data from Australia and the UK indicate no notable rise in prion disease incidence since the onset of COVID-19. According to reports, 148 individuals were diagnosed with probable or definite Creutzfeldt-Jakob Disease (CJD) during the pandemic, a figure not significantly different from the 141 cases recorded prior to it.
The possibility of COVID-19 acting as a precursor to prion diseases has been discussed in a handful of case reports from Italy, Iran, and the U.S. However, none of these reports provide compelling evidence of causation, leading to the suspicion that these occurrences could simply be coincidental.
Implications of COVID-19 Vaccines on Prion Diseases
Once a connection between COVID-19 and prion diseases is proposed, it is not long before COVID-19 vaccines are implicated, especially by anti-vaccine advocates. Several papers, many of which are not published in reputable journals, have explored this theory.
One such study titled "COVID-19 RNA Based Vaccines and the Risk of Prion Disease" claimed that specific sequences in the Pfizer mRNA vaccine could trigger pathological folding of proteins like TDP-43 and FUS into prion-like forms. However, this assertion hinges solely on a theoretical analysis of the mRNA sequence without any empirical data to back it up. The so-called "UG tandem repeats" mentioned in the study have not been proven to correlate with prion diseases in the existing literature.
Additionally, the author suggested that the spike protein generated from the vaccine may bind to the ACE2 enzyme, leading to increased intracellular zinc levels, which could, in turn, promote prion protein aggregation. If this reasoning were valid, it would imply that any substance interacting with ACE2 or elevating intracellular zinc—such as the COVID-19 virus itself or even dietary zinc—could potentially lead to prion diseases.
Ultimately, these interpretations are speculative and lack rigorous scientific validation, as noted by various experts.
Another paper, "Towards the emergence of a new form of the neurodegenerative Creutzfeldt-Jakob disease," analyzed 26 cases of prion diseases that appeared shortly after COVID-19 vaccinations in Europe. Symptoms emerged, on average, 11.4 days post-vaccination, with a significant number of cases resulting in death within a few months. The authors claim this rapid onset suggests a new variant of CJD, as the classic form typically manifests over decades.
However, establishing causation based on mere temporal association—such as the interval between vaccination and CJD symptom onset—is unconvincing. This situation mirrors the earlier case reports linking post-COVID-19 prion diseases, where causation remains uncertain.
While the case reports concerning post-COVID-19 prion diseases are published in credible journals, the data regarding post-vaccine cases largely derive from electronic records, particularly the Vaccine Adverse Event Reporting System (VAERS), which relies on voluntary reporting. In fact, some reported cases were not formally diagnosed with prion diseases but were merely assumed based on symptomatic similarities.
The assertion that these post-vaccine cases represent a novel form of prion disease due to their quick onset is questionable. Prion diseases generally exhibit long incubation periods; for instance, variant CJD can take 10–20+ years to manifest after exposure to contaminated sources. Even sporadic CJD, the most prevalent type, tends to occur spontaneously in older adults.
Most of the 26 post-vaccine CJD cases occurred in individuals aged 60 and older, a demographic already at risk for spontaneous CJD. Thus, it's plausible that these cases are simply instances of sporadic CJD unrelated to vaccination. Given that a significant proportion of older adults have been vaccinated, it stands to reason that some will inevitably develop CJD or prion diseases, purely by chance.
Moreover, the authors failed to conduct statistical analyses comparing the rates of prion diseases or CJD among vaccinated versus unvaccinated individuals to substantiate their claims. While this specific analysis is lacking, the Australian and UK surveillance data previously mentioned suggest that rates of CJD and prion diseases have remained relatively stable over time.
In conclusion, while the exploration of potential links between COVID-19, its vaccines, and prion diseases is ongoing, the current evidence does not support a causal relationship.
Insights From YouTube
To further investigate these connections, check out the following videos:
Video Title: Is There Any Relation Between the COVID-19 Vaccine and CJD?
Description: This video explores the potential connections between COVID-19 vaccines and Creutzfeldt-Jakob Disease (CJD), addressing common fears and misconceptions.
Video Title: Spike Protein an Engineered Prion Protein? - Kevin McCairn PhD
Description: In this video, Dr. Kevin McCairn discusses the implications of the spike protein and its potential to behave like a prion, scrutinizing the science behind this theory.
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