期刊
SCIENCE
卷 326, 期 5959, 页码 1546-1549出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1178849
关键词
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资金
- BIOTEC [BT-B06-MG-14-4507]
- Thailand Research Fund [BRG/16/2544]
- Mahidol University [OR-9123]
- Institut Pasteur program [PTR202]
- CNRS
- Agence Nationale de la Recherche (ANR) [ANR-05-JCJC-0124-01]
- Gates Grand Challenge program
- Wellcome Trust
- U. K. Medical Research Council
- Royal Golden Jubilee Program
- French Embassy in Thailand
- French Medical Research Foundation (FRM)
- Medical Scholar Program
- Mahidol University
Glucose-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-Mahidol(487A) 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-Mahidol(487A) 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.
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