Once it is in the cell, its signaling damages mitochondria. The team then replicated this process in the lab, exposing healthy endothelial cells (which line arteries) to the spike protein. They showed that the spike protein damaged the cells by binding ACE2. This binding disrupted ACE2’s molecular signaling to mitochondria (organelles that generate energy for cells), causing the mitochondria to become damaged and fragmented.

Once the mitochondria are damaged, this then activates the autoimmune response of the body. The accumulation of defective mitochondria led to overproduction of an inflammatory protein called type 1 interferon. The findings suggest that failed quality control of mitochondria may cause Sjogren’s, lupus, and other autoimmune diseases through production of interferon.

The Spike Protein then proceeds to travel from cell to cell via EXTRACELLULAR VESICLES. This means, of course, they will NOT BE FOUND IN THE BLOOD. We would not have been aware all this time. As the S1 unit has been found in monocytes 15 months post infection, it may be traveling intracellularly, executing a “Sherman’s March Through Georgia” on the mitochondria, resulting in multisystemic autoimmunity.

Again, we have known the spike enters cells via endocytosis since 2008.