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
https://jimmunol.org/content/181/12/8323
4. Regulation of autoimmune myocarditis by protein ubiquitination
https://jian-zhang.lab.uiowa.edu/4-regulation-autoimmune-myocarditis-protein-ubiquitination
SARS-CoV-2 Spike Protein Interacts with Multiple Innate Immune Receptors
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7402034/
Abnormal expression and function of Dectin-1 receptor in type 2 diabetes mellitus patients with poor glycemic control (HbA1c>8%)
https://pubmed.ncbi.nlm.nih.gov/22560862/