September 15, 2021
THE SPIKE WILL NOT BE FOUND IN THE BLOOD. IT IS TRAVELLING
“INCOGNITO” VIA EXTRACELLULAR VESICLES.
WE KNEW IT ENTERED CELLS VIA ENDOCYTOSIS IN 2008!
I observed that every cell the Spike Protein invades seems to cause the body to develop autoimmunity against it. I believe I have discovered the mechanism.
It is a very brief and straightforward mechanism.
Most likely many spikes do NOT stay on the cell surface, once they are expressed via spike protein therapied. The Spike is proven to be brought into the cell by Endocytosis. The spike protein is internalized into cells rapidly and is detected in cells within 5 mi, a hallmark of endocytosis. The amount of spike protein in cells continues to increase for up to 30 min. Thus, SARS-CoV-2 spike protein enters cells via endocytosis.
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.
SARS-CoV-2 infects cells after viral entry via clathrin-mediated endocytosis
THE NOVEL CORONAVIRUS’ SPIKE PROTEIN PLAYS ADDITIONAL KEY ROLE IN ILLNESS
Autoimmunity origins may lie in defective mitochondria
Persistence of SARS CoV-2 S1 Protein in CD16+ Monocytes in Post Acute Sequelae of COVID-19 (PASC) Up to 15 Months Post-Infection
Endothelial cell damage is the central part of COVID-19 and a mouse model induced by injection of the S1 subunit of the spike protein
Extracellular vesicles carry SARS-CoV-2 spike protein and serve as decoys for neutralizing antibodies