Figure 3.

Hepatitis C virus has several effects on anticoagulant and procoagulant cascades, in addition to the effects on coagulation derived from liver cirrhosis development. (1) Hepatitis C virus (HCV) infection is associated with anticardiolipin antibodies which are related to thrombotic events; (2) Viral HCV RNA binds to toll-like receptors (TLR)-3 found in endothelial cells which leads to inflammation. Also, HCV infection is associated with cryoglobulinemia and thus immune complexes directed against viral RNA are formed. Inflammation generated by these two mechanisms lead to TNF-α secretion. TNF-α is an inducer of tissue factor expression, therefore exerting a prothrombotic effect by activating the coagulation cascade and also downregulates thrombomodulin expression; and (3) In HCV infection, CXCL12 is up-regulated in the endothelium of blood vessels formed in active inflammatory foci. CXCL12 is a potent promoter of platelet aggregation and adhesion.