PMC8712467_01
Possible underlying mechanism of PVT by COVID-19 infection. Cholangiocyte is a kind of liver cell which has ACE II receptors presented on the surface more than hepatocytes and endothelium. By direct fusing of COVID-19 to these cells, first the direct injury of the liver happens because of the accumulation of bile acids. Then several inflammatory cytokines (IL6, TNF-alpha) are secreted and they play as inflammation and thrombosis triggers in the liver. Clot formation in the portal vein might be because of the increased expression of tissue factor (TF) from mononuclear cells, possibly done by IL-6. Beside this, other inflammatory cytokines such as tumor necrosis factor alpha (TNF-alpha) and IL-1 can play roles in anticoagulant pathway inhibition.
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ACE-2 receptors on the surface of cholangiocytes so the local presentation of COVID-19 in the liver, makes the body to produce different cytokines against it, which leads to the liver injury (Figure 2). As portal vein is a vital part of the liver, the thrombosis may be formed because of the same reason.
Similar to HIT, vaccine induced thrombocytopenia and thrombosis (VITI) occurs because of free DNA available in COVID-19 vaccines. The free DNA stimulates the production of PF-4 molecules from platelets. The PF4-free DNA attaches to FCRYll on the surface of platelets and the platelet clot shapes.
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HIT, the decreased counts of platelets are supposed to observe (Figure 3). However, in a 62-year-old woman with PVT that was reported by Graca (mentioned in