Where chloroquine still works: the genetic make-up and susceptibility of Plasmodium vivax to chloroquine plus primaquine in Bhutan

This was posted on Monday, May 16th, 2016 By in Publication

More than 2.8 billion people are reported to be at risk of Plasmodium vivax infection worldwide [1, 2], the number of reported infections ranging from 19 to 240 million cases each year [3]. As the incidence of Plasmodium falciparum decreases in many areas of Asia, P. vivax has emerged as the more prominent species. P. vivax exhibits important biological differences from P. falciparum, including the development of dormant liver stages and the emergence of gametocytes before the onset of clinical symptoms [4]. These properties afford the parasite greater transmission potential relative to P. falciparum, posing a challenge to control efforts and rendering P. vivax highly prone to resurgence. Furthermore P. vivax also exhibits greater genetic diversity than P. falciparum [5–8], enhancing the potential for P. vivax strains with adaptive genetic backgrounds to emerge in response to environmental challenges, such as anti-malarial drugs or host immune pressure. The large burden of low density P. vivax infections presents a diagnostic challenge, further impeding containment efforts [9].
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