The role of G-quadruplexes, exosomes, and MicroRNAs
Food and Chemical Toxicology | June 2022
Highlights
- • mRNA vaccines promote sustained synthesis of the SARS-CoV-2 spike protein.
- • The spike protein is neurotoxic, and it impairs DNA repair mechanisms.
- • Suppression of type I interferon responses results in impaired innate immunity.
- • The mRNA vaccines potentially cause increased risk to infectious diseases and cancer.
- • Codon optimization results in G-rich mRNA that has unpredictable complex effects.
Abstract
The mRNA SARS-CoV-2 vaccines were brought to market in response to the public health crises of Covid-19. The utilization of mRNA vaccines in the context of infectious disease has no precedent. The many alterations in the vaccine mRNA hide the mRNA from cellular defenses and promote a longer biological half-life and high production of spike protein. However, the immune response to the vaccine is very different from that to a SARS-CoV-2 infection. In this paper, we present evidence that vaccination induces a profound impairment in type I interferon signaling, which has diverse adverse consequences to human health. Immune cells that have taken up the vaccine nanoparticles release into circulation large numbers 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 potentially have a causal link to neurodegenerative disease, myocarditis, immune thrombocytopenia, Bell’s palsy, liver disease, impaired adaptive immunity, impaired DNA damage response and tumorigenesis. We show evidence from the VAERS database supporting our hypothesis. We believe a comprehensive risk/benefit assessment of the mRNA vaccines questions them as positive contributors to public health.
Innate immune suppression by SARS-CoV-2 mRNA vaccinations
Source: https://www.sciencedirect.com/science/article/pii/S027869152200206X