
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)!
https://arthritis-research.biomedcentral.com/articles/10.1186/s13075-016-1203-y
https://pubs.rsna.org/doi/full/10.1148/radiol.2021204482
https://sciencedaily.com/releases/2020/11/201104001307.htm