Figure 1.

Mechanisms of SARS-CoV-2-induced thrombosis in severe COVID-19. The binding of spike protein to the ACE2 receptor site indirectly triggers several downstream events, including the activation of the complement pathway, endothelial injury, and vasoconstriction. Complement proteins activate neutrophils, which then release neutrophil extracellular traps (NETs) that act as a platform for contact activation of the coagulation cascade. Vasoconstriction secondary to elevated angiotensin-II promotes clot formation, which eventually lead to site-specific thrombosis in severe COVID-19.