Why do viral infections lead to increased tissue factor (TF) expression?  What are the mechanisms of viral infection-induced TF expression? Is the TF induction a wanted response by the virus? Or is the TF induction the host’s own protective innate immune response? What happens when the TF induction is impaired? What happens when the TF induction is uncontrolled? Does TF act as initiator of coagulation or signaling? When TF is the start; what is the end product of the pathway? If signaling is involved, is it mediated through protease-activated receptors (PARs)? Which role has PAR4 in viral infections?

These are questions the Antoniak Lab wants to answer. We focus on pulmonary viral infections like influenza A virus and coronaviruses and on cardiac infections like viral myocarditis. We want to understand the life-supporting side of TF in hemostasis but also life threatening-side of TF in thrombosis. How can we support the good and limit the bad?

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