Malaria that is caused by Plasmodium falciparum is a significant global health problem. Genetic characteristics of the host influence the severity of disease and the ultimate outcome of infection, and there is evidence of coevolution of the plasmodium parasite with its host. In humans, pyruvate kinase deficiency is the second most common erythrocyte enzyme disorder. Here, we show that pyruvate kinase deficiency provides protection against infection and replication of P. falciparum in human erythrocytes, raising the possibility that mutant pyruvate kinase alleles may confer a protective advantage against malaria in human populations in areas where the disease is endemic.
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From the McLaughlin–Rotman Centre for Global Health (K.A., L.S., M.C., K.C.K.) and the Department of Medicine (I.Q., K.C.K.), University Health Network–Toronto General Hospital; Hematological Unit, Hospital for Sick Children (M.K.-A.); and the McLaughlin Centre for Molecular Medicine, University of Toronto (K.C.K.) — all in Toronto; and the Department of Biochemistry and Centre for the Study of Host Resistance, McGill University, Montreal (G.M.-O., P.G.).
This article (10.1056/NEJMoa072464) was published at www.nejm.org on April 16, 2008.
Address reprint requests to Dr. Gros at the Department of Biochemistry, McGill University, 3655 Promenade Sir William Osler, Rm. 907, Montreal, QC H3G 1Y6, Canada, or at philippe.gros{at}mcgill.ca.
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