Procoagulant activity during viral infections.

The abundance of evidence suggest that inflammation of immune and non-immune cells may lead to an imbalance of the pro- and anti-coagulant state during viral infections. During systemic infections, the endothelium plays a critical role in regulating hemostasis, and severe imbalances of endothelial function and activation can contribute to organ failure. Viral infections may elevate plasma levels of procoagulant markers such as TAT and D-dimer TF-positive MPs as well as von Willebrand factor (vWF). Although multiple clinical studies are showing the association of viral infection and increased prothrombotic risk, the pathological mechanisms have not been fully identified for most viral infections. Viral infection mediated TLRs activation is both cell type- and species-specific and explains the difficulties in correlating murine model data with the human data. In this review, we briefly discuss the TF-dependent coagulation activation, Toll-like receptors (TLRs) signaling during viral infections, and their contributions to the procoagulant response.