Myocarditis from SARS-CoV-2 Vaccination is Caused by Cell Fusion Caused Spike Protein

While articles from Reuters and Factcheck.org from June claim otherwise, yes, the SARS-CoV-2 virus can cause cell fusion… that is, the fusion of two different cells. That makes the spike protein itself pathogenic.

Due to the misinformation spread by Reuters and FactCheck.org, the denial of the risk of myocarditis following SARS-CoV-2 vaccination continues even now - and indeed seems to be ramping up. So I though I would share with you the key references that demonstrate cell-cell fusion (syncytia) and implicate the spike protein as a pathogenic molecule as the cause. That is, the protein, not the virus, is the pathogen.

Note that many of these reference implications for SARS-CoV-2 infection, but the same conclusion applies to injection: the mechanistic studies do not use the virus, they use virus-like-particles (VLPs) with spike protein on the surface. Thus, the findings and conclusions of such studies apply equally well to vaccines that induce spike protein.

With conclusions such as “The SARS-CoV-2 spike protein can directly produce cellular damage” and “These data indicate that SARS-CoV-2 may cause cardiac damage by fusing cardiomyocytes”, the continued denial of vaccine causality must end, the so-called Fact-Checkers (aka “Narrative Minders” - thank you M.K. for that) - should retract their articles and issue apologies to the families and individuals hurt by vaccine-induced myocarditis as a result of their misinformation campaigns.

1. Highly Efficient SARS-CoV-2 Infection of Human Cardiomyocytes: Spike Protein-Mediated Cell Fusion and Its Inhibition (Link)

Navaratnarajah CK, Pease DR, Halfmann PJ, Taye B, Barkhymer A, Howell KG, Charlesworth JE, Christensen TA, Kawaoka Y, Cattaneo R, Schneider JW; Wanek Family Program for HLHS-Stem Cell Pipeline. Highly Efficient SARS-CoV-2 Infection of Human Cardiomyocytes: Spike Protein-Mediated Cell Fusion and Its Inhibition. J Virol. 2021 Nov 23;95(24):e0136821. doi: 10.1128/JVI.01368-21. Epub 2021 Oct 6. PMID: 34613786; PMCID: PMC8610601.

Abstract

Severe cardiovascular complications can occur in coronavirus disease of 2019 (COVID-19) patients. Cardiac damage is attributed mostly to the aberrant host response to acute respiratory infection. However, direct infection of cardiac tissue by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) also occurs. We examined here the cardiac tropism of SARS-CoV-2 in spontaneously beating human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs). These cardiomyocytes express the angiotensin-converting enzyme 2 (ACE2) receptor but not the transmembrane protease serine 2 (TMPRSS2) that mediates spike protein cleavage in the lungs. Nevertheless, SARS-CoV-2 infection of hiPSC-CMs was prolific; viral transcripts accounted for about 88% of total mRNA. In the cytoplasm of infected hiPSC-CMs, smooth-walled exocytic vesicles contained numerous 65- to 90-nm particles with canonical ribonucleocapsid structures, and virus-like particles with knob-like spikes covered the...

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