Chalisa LouicharoenEtienne PatinRichard PaulIssarang NuchprayoonBhee WitoonpanichChayanon PeerapittayamongkolIsabelle CasademontThanyachai SuraNan M. LairdPratap SinghasivanonLluis Quintana-MurciAnavaj SakuntabhaiInstitut Pasteur, ParisChulalongkorn UniversityCNRS Centre National de la Recherche ScientifiqueMahidol UniversityHarvard School of Public HealthInserm2018-09-132018-09-132009-12-11Science. Vol.326, No.5959 (2009), 1546-154910959203003680752-s2.0-72149127949https://repository.li.mahidol.ac.th/handle/20.500.14594/27789Glucose-6-phosphate dehydrogenase (G6PD) deficiency - the most common known enzymopathy - is associated with neonatal jaundice and hemolytic anemia usually after exposure to certain infections, foods, or medications. Although G6PD-deficient alleles appear to confer a protective effect against malaria, the link with clinical protection from Plasmodium infection remains unclear. We investigated the effect of a common G6PD deficiency variant in Southeast Asia-the G6PD-Mahidol487A variant - on human survival related to vivax and falciparum malaria. Our results show that strong and recent positive selection has targeted the Mahidol variant over the past 1500 years. We found that the G6PD-Mahidol487A variant reduces vivax, but not falciparum, parasite density in humans, which indicates that Plasmodium vivax has been a driving force behind the strong selective advantage conferred by this mutation.Mahidol UniversityMedicineMultidisciplinaryArticleSCOPUS10.1126/science.1178849