In silico modelling of all available data shows that a twenty-day ascending-dose primaquine regimen could be safe to administer to G6PD deficient patients for the radical cure of vivax malaria.

Increasing levels of glucose-6-phosphate dehydrogenase deficiency are associated with decreasing risk of cerebral malaria, but with increased risk of severe malarial anaemia.

The Mediterranean variant of glucose-6-phosphate dehydrogenase deficiency confers a strong gene-dose proportional protective effect against symptomatic Plasmodium vivax malaria in the Pashtun ethnic group.

A full radical curative dose of primaquine can be given to fully glucose-6-phosphate dehydrogenase-deficient males safely using an ascending dose regimen.

We are writing to comment on the article by Watson et al., 2022 about the antimalarial drug tafenoquine.

Selection bias, also known as collider bias, likely explains the apparent protective effect of G6PD deficiency against cerebral falciparum malaria.

We are writing to respond to comment by Sharma et al, 2024 on our article about the antimalarial drug tafenoquine.

6-Phosphogluconate dehydrogenase controls regulatory T cells metabolism with shifts to Th1, Th2, and Th17 phenotypes.

The currently recommended adult dose of tafenoquine is insufficient for radical cure in all adults.

Strongly protective effect conferred by the Dantu blood group variant against early, non-clinical, Plasmodium falciparum malaria infections in vivo.