June 28, 2021

The Spike Protein of SARS-CoV-2 has been found to bind to several additional receptors other than ACE-2. Dectin-1 is one of those additional receptors that the S1 unit of the Spike Protein binds to.

I believe that the S1 unit is being cleaved in Spike Protein experimental therapies and binding to Dectin-1 (among other receptors). This binding to Dectin-1 downregulates the expression of Dectin-1 which is implicated in the pathogenesis of Myocarditis and Diabetes.

It is also possible that this binding is causing toxification of Dectin-1 and autoantibodies may develop. This could explain the incidences of Mucormycosis, as Dectin-1 is a primary antifungal signaling protein. 

Note that monocytes from T2D patients with poor glycemic control (HbA1c>8%) showed a diminished percentage of Dectin-1(+)/TLR2(+) cells. Negative correlations between the percent of Dectin-1(+)/TLR2(+) cells and fasting plasma glucose levels (FPG) and HbA1c levels were found. 

Please note that the referenced Myocarditis article refers to Myocarditis as a “devastating heart disease." No such thing as a “mild case of Myocarditis." Yet another lie.

Referenced/Related Papers

Induction of Innate Immune Response through TLR2 and Dectin 1 Prevents Type 1 Diabetes

4. Regulation of autoimmune myocarditis by protein ubiquitination

SARS-CoV-2 Spike Protein Interacts with Multiple Innate Immune Receptors

Abnormal expression and function of Dectin-1 receptor in type 2 diabetes mellitus patients with poor glycemic control (HbA1c>8%)