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THE SPIKE PROTEIN SUPERANTIGEN, MYOCARDITIS AND MORTALITY
DOCTORS MUST NOW PROTEST THE SPIKE PROTEIN ACCELERANT BEING THROWN ON THE SARS-CoV-2 FIRE
I am shocked and dismayed that the medical community has not addressed the massive elephant (among many) in the room regarding the appearance of Myocarditis. As I have previously stated, I believe that the incidence of Myocarditis is widespread in those exposed to the Spike Protein of SARS-CoV-2.
A major component of this pathology is the fact that the Spike Protein is a Superantigen. It has been shown that the SARS-CoV-2 spike contains sequence and structure motifs highly similar to those of a bacterial superantigen and may directly bind T cell receptors.
But what does this mean for Myocarditis? Everything.
A parallel may be found in Coxsackievirus B, another virus with a Superantigen. A superantigen-mediated immune response is involved in human heart disease. CVB3 may directly or indirectly trigger this response, suggesting a possible mechanistic link between CVB infection and myocarditis development progressing to IDC.
Quite frankly, when you are told that Myocarditis is “mild” you are being told a boldfaced lie. Nothing could be farther from the truth.
Let us look at what ACTUALLY happens when Myocarditis is caused by a Superantigen.
Myocarditis exhibits a wide spectrum of clinical manifestations, ranging from essentially asymptomatic, transient inflammation to severe congestive heart failure, dysrhythmias, and death. The overall prognosis of myocarditis in children remains poor. In a comprehensive study, only 7 of 34 patients (21%) had resolution of their illness. Despite intensive support, the overall mortality was 62%. Furthermore, myocarditis is a major cause of sudden, unexpected death in adults <40 years old, with ≈20% of such individuals dying of this disease. There is substantial evidence that viral and/or inflammatory myocarditis can progress to IDC,3 which, second to ischemic heart disease, is the most common indication for heart transplantation.
We must autopsy all sudden cardiac deaths in the young using nuclear imaging technology as only this will fine the microvascular damage the Spike Protein has caused leading to Myocarditis.
The connection should be obvious: Superantigenic character of an insert unique to SARS-CoV-2 spike supported by skewed TCR repertoire in patients with hyperinflammation. And the parallel with Coxsackievirus B: The ability of lysates from CVB3-infected Vero cells to stimulate in vitro T cells from healthy donors carrying the same 3 TCR Vβ families we have found skewed in vivo (ie, Vβ3, 7, and 13.1) further supports the hypothesis of a superantigen-driven immune response.
The only path forward is for doctors to unite and stop the use of the Spike Protein Accelerant on the SARS-CoV-2 fire. Unfortunately, that is only a first step. Dealing with a virus to which no lasting immunity can be generated may indeed be very bad news for the human race.