Stephanie Seneff 1*, Anthony M Kyriakopoulos2, Greg Nigh3Senior Research Scientist, Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology, Cambridge MA USA; [email protected] and Head of Research and Development, Nasco AD Biotechnology Laboratory, Department of Re-search and Development, Sachtouri 11, 18536, Piraeus, Greece; [email protected] Oncologist, Immersion Health, Portland, OR 97214, USA; [email protected].* Corresponding author: Stephanie Seneff. Email: [email protected].

The SARS-CoV-2 spike protein and prions use common pathogenic pathways to induce toxicity in neurons. Infectious prions activate the p38 mitogen activated protein kinase (MAPK) pathway, and SARS-CoV-2 spike proteins induce the p38 MAPK and c-Jun NH2-terminal kinase (JNK) pathways through toll-like receptor signaling, indicating the potential for similar neurotoxicity, causing prion and prion-like disease. In this review we analyze the roles of autophagy inhibition, elevated intracellular p53 levels and reduced Wild-type p53-induced phosphatase 1 (Wip1) and dual-specificity phosphatase (DUSP) expression in neurons. The pathways induced by the spike protein via toll like receptor activation induce both PrPC upregulation and β amyloid expression. Through the spike-protein-dependent elevation of p53 levels via β amyloid metabolism, increased PrPC expression can lead to PrP misfolding and impaired autophagy, generating prion disease. We conclude that, according to the age of the spike protein-exposed patient and the state of their cellular autophagy activity, excess sustained activity of p53 in neurons may be a catalytic factor in neurodegeneration. We conclude that neurodegeneration is in part due to intensity and duration of spike protein exposure, patient age, cellular autophagy activity, and activation, function and regulation of p53. Finally, the neurologically damaging effects can be cumulatively spike-protein dependent, whether exposure is by natural infection or, more substantially, by repeated mRNA vaccination.

The mRNA SARS-CoV-2 vaccines were brought to market in response to the widely perceived public health crises of Covid-19. The utilization of mRNA vaccines in the context of infectious disease had no precedent, but desperate times seemed to call for desperate measures. The mRNA vaccines utilize genetically modified mRNA encoding spike proteins. These alterations hide the mRNA from cellular defenses, promote a longer biological half-life for the proteins, and provoke higher overall spike protein production. However, both experimental and observational evidence reveals a very different immune response to the vaccines compared to the response to infection with SARS-CoV-2. As we will show, the genetic modifications introduced by the vaccine are likely the source of these differential responses. In this paper, we present the evidence that vaccination, unlike natural infection, induces a profound impairment in type I interferon signaling, which has diverse adverse consequences to human health. We explain the mechanism by which immune cells release into the circulation large quantities of exosomes containing spike protein along with critical microRNAs that induce a signaling response in recipient cells at distant sites. We also identify potential profound disturbances in regulatory control of protein synthesis and cancer surveillance. These disturbances are shown to have a potentially direct causal link to neurodegenerative disease, myocarditis, immune thrombocytopenia, Bell’s palsy, liver disease, impaired adaptive immunity, increased tumorigenesis, and DNA damage. We show evidence from adverse event reports in the VAERS database supporting our hypothesis. We believe a comprehensive risk/benefit assessment of the mRNA vaccines excludes them as positive contributors to public health, even in the context of the Covid-19 pandemic.    

Background The findings of a sequence embedded in Human DNA that was almost identical to a sequence in the SARS-CoV-2 genome, and the identification of plausible integration of SARS-CoV-2 RNA into human DNA by endogenous reverse transcriptase activity expressed by Long Interspersed Nuclear Element (LINE)-1 (17% of Human DNA) have raised concerns about the long-term safety of messenger-RNA (mRNA) based vaccination. Recent data demonstrate that SARS-CoV-2 RNA sequences can be transcribed into DNA and may be actively integrated into the genome of affected human cells, mediated by retrotransposons. Complementarily, in some SARS-CoV-2 infected patient specimens, there is evidence for a large fraction SARS-CoV-2 sequence integration and subsequent generation of SARS-CoV-2-human chimeric transcripts. 2 Results In this review, the potential role of mobile genetic elements in the etiopathogenesis of cardiovascular, neurological, immunological, and oncological disease and the possibilities of human DNA interference by SARS-CoV-2 vaccination are repositioned. Vulnerable human stem cells as well as gametocytes can presumably be the first targets for unwanted RNA interference. Given the many genetic manipulations of the RNA coding for the SARS-CoV-2 spike glycoprotein in the vaccines, manipulations designed to increase stability and efficiency of spike protein translation, much remains uncertain about the potential disruptions to cellular physiology and homeostasis that could ensue. The predicted consequences pose serious risks to human health that are in need of clarification. Conclusion Further toxicity evaluations are urgently needed to quantify potential emergence of interference with canonical DNA processes that could detrimentally impact the mRNA-vaccinated population.

Human prion protein and prion-like protein misfolding are widely recognized as playing a causal role in a large and growing number of neurodegenerative diseases. Here we summarize the compelling evidence that the spike protein of SARS-CoV-2 contains extended amino acid sequences previously established as characteristic of a prion-like protein. This suggests that vaccine-induced spike protein production is synonymous with production of a prion-like protein, and we trace some of the various pathways through which these proteins should be expected to traverse and distribute throughout the body. We describe some of the highly concerning biological consequences that would be expected to occur with increased frequency as a consequence. Specifically, we describe spike-protein contribution, via its prion-like properties, to neuroinflammation and neurodegenera-tive diseases; to clotting disorders within the vasculature; to suppressed prion protein regulation in the context of widely prevalent insulin resistance; and other health complications it could be expected to induce. We explain why these prion-like characteristics are more relevant to vaccine-related mRNA-induced spike proteins than natural infection with SARS-CoV-2. We conclude with some potentially ominous public health implications and recommendations for investigations of these possibilities.