Asian G6PD-Mahidol Reticulocytes Sustain Normal Plasmodium Vivax Development

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common enzymatic disorder in humans and appears to be protective against falciparum severe malaria. Controversially, it is also thought that Plasmodium vivax has driven the recent selection of G6PD alleles. We use an experimental approa...

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Detalles Bibliográficos
Autores principales: Bancone, Germana, Malleret, Benoit, Suwanarusk, Rossarin, Chowwiwat, Nongnud, Chu, Cindy S, McGready, Rose, Rénia, Laurent, Nosten, François, Russell, Bruce
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2017
Materias:
Brief Reports
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5853331/
https://www.ncbi.nlm.nih.gov/pubmed/28591790
http://dx.doi.org/10.1093/infdis/jix278
Descripción
Sumario:Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common enzymatic disorder in humans and appears to be protective against falciparum severe malaria. Controversially, it is also thought that Plasmodium vivax has driven the recent selection of G6PD alleles. We use an experimental approach to determine whether G6PD-Mahidol(G487A) variant, a widespread cause of severe G6PD deficiency in Southeast Asia, provides a barrier against vivax malaria. Our results show that the immature reticulocytes (CD71(+)) targeted by P. vivax invasion are enzymatically normal, even in hemizygous G6PD-Mahidol (G487A) mutants; thus, allowing the normal growth, development, and high parasite density in severely deficient samples.

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