Open AccessGlucose-6-phosphate dehydrogenase deficiency inhibits in vitro growth of Plasmodium falciparum.
Author(s) -
Elizabeth Röth,
Carmen Raventós-Suárez,
A Rinaldi,
Ronald L. Nagel
Publication year - 1983
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.80.1.298
Subject(s) - heterozygote advantage , hemolysis , glucose 6 phosphate dehydrogenase deficiency , plasmodium falciparum , biology , glucosephosphate dehydrogenase deficiency , malaria , glucose 6 phosphate dehydrogenase , thalassemia , in vitro , immunology , dehydrogenase , genetics , gene , endocrinology , biochemistry , enzyme , genotype
Glucose-6-phosphate dehydrogenase (G6PD; EC 1.1.1.49)-deficient red blood cells from male hemizygotes and female heterozygotes from the island of Sardinia were studied for their ability to support growth in vitro of the malaria-causing organism Plasmodium falciparum. Parasite growth was approximately one-third of normal in both hemi- and heterozygotes for G6PD deficiency. In Sardinians with the beta 0-thalassemia trait, parasite growth was normal except when G6PD deficiency occurred together with the thalassemia trait. The data support the hypothesis that G6PD deficiency may confer a selective advantage in a malarious area; the female heterozygote may be at a particular advantage because resistance to malaria equals that of male hemizygotes, but the risk of fatal hemolysis may be less. However, more female heterozygotes must be studied to confirm this hypothesis. No protective effect of beta 0-thalassemia trait could be demonstrated in vitro.