Abstract
IT is thought that the deleterious properties of thalassaemia (thal) and glucose-6-phosphate dehydrogenase deficiency (G6PD−) are balanced in the population by a conferred protection against malaria, and that some characteristic of the variant red cell acts directly to inhibit the invasion or intracellular development of the malaria parasite. Indeed, such is the case for sickle cell disorders1,2. Recently, Pasvol et al.3, having shown that fetal haemoglobin (HbF) (in both fetal and adult cells) inhibits malaria parasite development, have suggested that the slight persistance of HbF in children with thal trait is responsible for the selective advantage of the thal gene. They have reported no difference in parasite development in the red cells of adult carriers of thal. Evidence is presented here that both α- and β-thal trait red cells from adults are refractory to parasite development because of oxidant sensitivity, and, furthermore, that fetal red cells and G6PD− cells are refractory for the same reason.
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FRIEDMAN, M. Oxidant damage mediates variant red cell resistance to malaria. Nature 280, 245–247 (1979). https://doi.org/10.1038/280245a0
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DOI: https://doi.org/10.1038/280245a0
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