There appears to be an intimate associate between the spike protein and clotting. Especially microclotting, which has been obeserved in the alveoli of severe covid. There have been strokes and heart attacks even in asymptomatic cases.
However, what are the mechanisms of this connection? One very important clue is the role of Interstitial Lung Disease. The spike protein has been proven to cause synctia in the lung. Patients showed extensive blood clotting of the lung arteries and veins (thrombosis). Second, several lung cells were abnormally large and had many nuclei, resulting from the fusion of different cells into single large cells. This formation of fused cells (syncytia) is due to the viral spike protein, which the virus uses to enter the cell. When the protein is present on the surface of cells infected by the COVID-19 virus, it stimulates their fusion with other normal lung cells, which can be a cause for inflammation and thrombosis.
This leads to Interstital Lung Disease in many survivors. Many survivors with severe infection have long-term residual abnormalities on their thoracic CT scans, but current studies do not extend follow-up beyond 6 months. Residual pulmonary disease is sometimes referred to as “post-COVID interstitial lung disease” (ILD).
In Intersitial Lung Disease, Platelet Factor 4 (CLCX4) is significantly upregulated. This can explain the presence of autoantibodies to Platelet Factor 4 found in the cases of clotting associated with post-spike protein therapies.
The questions are many. Are synctia being formed by the spike post-spike protein therapy? Are the lungs being morphologically affected by the spike? Because Respiratory Synctial Virus exhibits overexpression of CXCL4 (previously known as platelet factor 4)!