SPIKE PROTEIN, TLR2/MyD88 AND TUMORIGENESIS

March 18, 2021

SPIKE PROTEIN INTERACTIONS WITH TLR2/MyD88 AND TLR4 ARE IDEAL FOR INDUCING TUMORIGENESIS

A paper out recently shows that the Spike Protein induces inflammation via TLR2-dependent activation of the NF-κB pathway. Biochemical studies revealed that S protein triggers inflammation via activation of the NF-kB pathway in a MyD88-dependent manner. This combined with another recent paper demonstrating that the Spike Protein interacts with and activates TLR4 allow for a most potent signaling cascade for the induction of carcinogenesis. 

This may explain why the virus presents more as a bacterium, as bacteria are more suited to creating this carcinogenic signaling pathway. TLR4 signaling also is involved in the induction/severity of Cancer Cachexia. Once again, I believe the Robust Immune Response created by the mRNA therapies in no way compensate for the (deliberate) carcinogenic effects of the spike protein’s intracellular signaling.

Referenced/Related Papers

SARS-CoV-2 spike protein interacts with and activates TLR4 

https://biorxiv.org/content/biorxiv/early/2020/12/18/2020.12.18.423427.full.pdf

The Yin and Yang of Toll-like receptors in cancer

https://nature.com/articles/onc2013302

SARS-CoV-2 spike protein induces inflammation via TLR2-dependent activation of the NF-κB pathway

https://www.biorxiv.org/content/10.1101/2021.03.16.435700v1