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At the end of World War I, British medical officers noted that soldiers infected with malaria were more likely to die during the 1918 influenza pandemic than those without malaria. This synergistic mortality appeared to be specific to Plasmodium falciparum and has not been generally noted since 1920. A possible explanation is that a malaria-induced procoagulant state enhanced the activation of influenza virus to increase inflammation and subsequent severe clinical outcomes. Falciparum proteins bind and likely inhibit antithrombin 3 and other factors. Pathogens interact in ways that may inform pathophysiology studies of remote epidemics.
Financial support: G. Dennis Shanks is an employee of the Australian Defence Force and received support for influenza studies from the Armed Forces Health Surveillance Center of the U.S. Department of Defense, Silver Spring, MD.
Author's addresses: G. Dennis Shanks, Australian Army Malaria Institute, Enoggera, Australia, University of Queensland, School of Population Health, Brisbane, Australia, and Department of Zoology, University of Oxford, Oxford, United Kingdom, E-mail: firstname.lastname@example.org.