Mechanisms
Recent introduction of mRNA vaccines that program human cells’ genetic mechanisms to generate spike proteins have led to an increased interface generally between spike proteins and bodily tissues. These recently increased venues of interaction have apparently exceeded, both in human populations and in human tissues, the levels that mRNA vaccine developers had expected. For unknown reasons, mRNA vaccine researchers had expected spike proteins to remain entirely in the deltoid muscle at the vaccination site of the vaccinated person, as reported in the media,
[12] and it was apparently imagined that these spike proteins could somehow evade release into the general circulation. However, it has recently been determined that the delivery of spike proteins and / or their generating mechanisms, as with all known injected substances, do indeed diffuse and travel in an organism, away from the site of injection, in accordance with well-established principles of circulation, throughout the body, including to internal organs. Organs that have been affected by this body-wide distribution have included the heart, brain, spleen and liver, with especially high concentrations found in the ovaries and the plasma.
[13]
The spike protein is the part of coronaviruses in general, and SARS-CoV-2 in particular, that attaches to and interacts with human cell membranes. I examine the role of the SARS-CoV-2 spike protein on the myocardium, and mechanisms by which the cardiomyocytes and vascular endothelial cells, which predominate there, may be threatened by such exposure. It is possible that other elements of the SARS-CoV-2 virus, besides spike proteins, have deleterious effects on cells, including risk for myocarditis.
[14] It has been observed also that mRNA interventions are fragile and unpredictable in their effect,
[15] and have been seen to damage mitochondria by a number of known mechanisms.
[16] Of patients hospitalized for COVID-19, myocarditis-pattern injury was observed in 4.5%
[17] to 27% of cases.
[18] Moreover, in the event of SARS-CoV-2 infection, it was found that the associated cytotoxic and pro-apoptotic effects were sufficient to abolish cardiomyocyte beating (contraction-relaxation cycles).
[19] However, direct virus replication was not found on examination of the myocardium,
[20] [21] and SARS-CoV-2 RNA was not found in the cardiomyocytes.
[22] Therefore, it is worthwhile to examine if post-vaccine myocarditis is likely to be caused by spike proteins generated by the vaccines, and to result from either the cytokine storm or from the endothelial damage caused by spike proteins. Considering a wider set of possible causes, we know that fulminant SARS-CoV-2 infection is characterized by hypoxia, systemic inflammation, thrombosis and / or cardiomyopathy, as well as myocarditis. All of these have been observed in vitro in the presence of spike proteins, and all of these can result in higher levels of measured troponin, which in turn establishes diagnosis of myocarditis, or at least clinical awareness of signs of myocarditis. [23]
At this time, there is not any other part of the SARS-CoV-2 virus that is known to attach to human cells. The binding of the spike protein to cell membranes initiates a cascade of events that result in fusion of the viral and cellular membranes and entry of the virus into the human cytoplasm. [24] Most of this activity in most human cells seems to involve one or both of the S1 subunits of the spike protein, but for human brain endothelial cells, it seems the S2 subunit of the spike protein is involved. [25] Human host cell proteases participate in this fusion and entry. [26]