Hemostasis in arenavirus infection

In this issue of Blood, Lafoux and colleagues(1) present a comprehensive study of mammarenavirus infection in cynomolgus macaques, a model for viral hemorrhagic fevers, analyzing the changes in hemostatic and platelet activation markers. Importantly, viral hemorrhagic fever infections are almost always associated with the activation of coagulation cascade and platelets, which can be due to the pathogen itself or can be a protective defensive host response to maintain hemostasis.(2,3) For instance, fibrin entrapment of bacteria is thought to be due to the host's response, but viral infections may also enhance fibrin depositions.(2) Although the virus itself might be too small to be entrapped in a fibrin network, viruses can interact with platelets. Platelets mediate viral clearance by engulfing them for destruction and thus limiting systemic viremia.(2,3)