Mitochondria Driven Autoinflammation

June 1, 2021

IS THE SPIKE PROTEIN OF SARS-CoV-2 IGNITING A SUPERANTIGEN FUSE DETONATING AN AUTOINFLAMMATORY BOMB?

The Spike Protein of the SARS-CoV-2 virus has been shown to cause damage to mitochondria via its interaction with ACE2. As mitochondrial components enter the extracellular space, the immune system misreads these components as an infectious agent. 

In addition to this, the Spike Protein’s antagonistic binding to a7nAChR receptors activates Mast Cells and contributes to their degranulation.

This explains why a Coronavirus (which before any of the SARS viruses appeared was, overall, quite harmless) has become the instigator of catastrphic immune events. It is because of the Spike Protein. I believe the Spike Protein has been engineered to 1) initiate an extreme inflammatory response on its own and then (in susceptible individuals, perhaps all if the Spike had been further refined) 2) TRANSITION that extreme EXOGENOUS inflammatory response to an extreme ENDOGENOUS inflammatory response, causing the body to destroy itself in devastating storm of cytokines. 

This “shifting of gears" so overwhelms the body that, very likely at this point, nothing can be done to save the victim. It is diabolically ingenious. I do not believe a natural virus would evolve to do this to its host. 

The sequlae of this one-two assault on the immune system could be Long COVID. Especially if the mitochondrial components have become toxified. 

Perhaps we should look for antibodies against mitochondria? This would explain much of Long COVID.

Referenced/Related Papers

Stimulated Human Mast Cells Secrete Mitochondrial Components That Have Autocrine and Paracrine Inflammatory Actions

https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0049767

IgE-induced degranulation of mucosal mast cells is negatively regulated via nicotinic acetylcholine receptors

https://pubmed.ncbi.nlm.nih.gov/18848921/

Neurotransmitter and neuropeptide regulation of mast cell function: a systematic review

https://jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-020-02029-3