Asian G6PD-Mahidol Reticulocytes Sustain Normal Plasmodium Vivax Development.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 28591790.
- Also identified by DOI 10.1093/infdis/jix278 and PMC identifier 5853331.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
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.
Medical subject headings
- Glucosephosphate Dehydrogenase
- Glucosephosphate Dehydrogenase Deficiency
- Malaria, Vivax
- Plasmodium vivax
- Reticulocytes