Abstract

An animal model of H1N1 influenza demonstrates that this infection is associated with pulmonary and systemic activation of coagulation and impairment of fibrinolysis in addition to systemic inflammation and intense neutrophil influx into the lung. Activated protein C attenuates coagulation activation and restores fibrinolytic capacity but has little effect on inflammation or survival from this infection. This animal model points to a profound inflammatory state developing in H1N1 infection that impacts mortality. Additional modifications to the model and the type and amount of activated protein C dosing will provide the data to determine the possible use of activated protein C as a therapy in human H1N1 infection.