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Natural selection of hemi- and heterozygotes for G6PD deficiency in Africa by resistance to severe malaria (1995)

Ruwende, C. ; Khoo, S. C. ; Snow, R. W. ; [et al.]

[s.l.] : Nature Publishing Group

Nature 376 (1995), S. 246-249

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ISSN: 1476-4687

Source: Nature Archives 1869 - 2009

Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics

Notes: [Auszug] Despite the extensive heterogeneity of G6PD deficiency, a single molecular variant, G6PD A-, seems predominant in sub-Saharan Africa12 14. It differs from the normal G6PD B allele at two amino-acid positions, one at position 376 encoding the B to A change and the other at position 202 that ...

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1038/376246a0

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Glucose-6-phosphate dehydrogenase deficiency and malaria (1998)

Ruwende, C. ; Hill, Adrian

Springer

Journal of molecular medicine 76 (1998), S. 581-588

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ISSN: 1432-1440

Keywords: Key words Glucose-6-phosphate dehydrogenase deficiency ; Severe malaria ; Protection ; Heterozygotes ; Hemizygotes

Source: Springer Online Journal Archives 1860-2000

Topics: Medicine

Notes: Abstract Glucose-6-phosphate dehydrogenase (G6PD) is a cytoplasmic enzyme that is essential for a cell’s capacity to withstand oxidant stress. G6PD deficiency is the commonest enzymopathy of humans, affecting over 400 million persons worldwide. The geographical correlation of its distribution with the historical endemicity of malaria suggests that 66PD deficiency has risen in frequency through natural selection by malaria. This is supported by data from in vitro studies that demonstrate impaired growth of P. falciparum parasites in G6PD-deficient erythrocytes. Attempts to confirm that G6PD deficiency is protective in field studies of malaria have yielded conflicting results, but recent results from large case control studies conducted in East and West Africa provide strong evidence that the most common African G6PD deficiency variant, G6PD A–, is associated with a significant reduction in the risk of severe malaria for both G6PD female heterozygotes and male hemizygotes. The effect of female homozygotes on severe malaria remains unclear but can probably be assumed to be similar to that of comparably deficient male hemizygotes.