May 30, 2021
Through the spike protein's interaction with ACE2, it disrupts mitochindrial signaling inducing ROS and oxidative stress. This results in mitochondrial fission, releasing the mitochondrial DNA into the cytoplasm and bloodstream.
The trauma created by the spike protein alone can trigger Systemic inflammatory response syndrome and Hauser et al. made the seminal observation that it is the freely circulating mtDNA following traumatic injury which possesses the distinct ability to trigger and drive the clinical manifestation of SIRS. The role for mtDNA in immune-mediated inflammatory diseases, unlike conditions relating to injury, is now also emerging. In rheumatoid arthritis, a chronic relapsing autoimmune condition affecting the joints, mtDNA was present in the plasma and synovial fluid of most patients but undetectable in healthy controls. Similarly, higher plasma mtDNA is found in granulomatosis with polyangiitis, an autoimmune disease whose features include necrotising granulomatous inflammation and vasculitis. Systemic lupus erythematosus (SLE) is a multi-organ autoimmune disease with hallmarks including excessive type I interferon (IFN) and antibodies against nucleic acids.
mtDNA CONTRIBUTES TO THE INFLAMMATORY RESPONSE, which means that the body may be "primed" to have a cytokine storm upon contact with a pathogen in the future.
mtDNA is also indicated in several cancers, including Lung, Breast, Ovarian and Testicular.
It is possible that the Spike Protein alone is causing significant mitochondrial damage. If the damage occurs in stable and/or permanent cells, the implications could be dire, indeed.
Referenced/Related Papers
Advances in the understanding of mitochondrial DNA as a pathogenic factor in inflammatory diseases
https://ncbi.nlm.nih.gov/pmc/articles/PMC5321122/
SARS-CoV-2 Spike Protein Impairs Endothelial Function via Downregulation of ACE 2
https://ahajournals.org/doi/10.1161/CIRCRESAHA.121.318902
COVID-19: A Mitochondrial Perspective