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Asian G6PD-Mahidol Reticulocytes Sustain Normal Plasmodium Vivax Development.

Authors :
Bancone, Germana
Malleret, Benoit
Suwanarusk, Rossarin
Chowwiwat, Nongnud
Chu, Cindy S.
McGready, Rose
Rénia, Laurent
Nosten, François
Russell, Bruce
Source :
Journal of Infectious Diseases. 7/15/2017, Vol. 216 Issue 2, p263-266. 4p.
Publication Year :
2017

Abstract

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-MahidolG487A 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. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
00221899
Volume :
216
Issue :
2
Database :
Academic Search Index
Journal :
Journal of Infectious Diseases
Publication Type :
Academic Journal
Accession number :
124462622
Full Text :
https://doi.org/10.1093/infdis/jix278