Abstract
Despite the high burden of Plasmodium vivax malaria in South Asian countries, the genetic diversity of circulating parasite populations is not well described. Determinants of antimalarial drug susceptibility for P. vivax in the region have not been characterised. Our genomic analysis of global P. vivax (n = 558) establishes South Asian isolates (n = 92) as a distinct subpopulation, which shares ancestry with some East African and South East Asian parasites. Signals of positive selection are linked to drug resistance-associated loci including pvkelch10, pvmrp1, pvdhfr and pvdhps, and two loci linked to P. vivax invasion of reticulocytes, pvrbp1a and pvrbp1b. Significant identity-by-descent was found in extended chromosome regions common to P. vivax from India and Ethiopia, including the pvdbp gene associated with Duffy blood group binding. Our investigation provides new understanding of global P. vivax population structure and genomic diversity, and genetic evidence of recent directional selection in this important human pathogen.
Highlights
Despite the high burden of Plasmodium vivax malaria in South Asian countries, the genetic diversity of circulating parasite populations is not well described
By evaluating samples from travellers returning to the UK with vivax malaria within the past 3 years, each with unambiguous travel histories to malaria-endemic countries, we have provided whole genome sequencing data for 132 P. vivax isolates
This result may arise because travellers are exposed to fewer infective bites than people living permanently in a malaria-endemic region over long periods of time, and on average are infected with fewer genotypes
Summary
Despite the high burden of Plasmodium vivax malaria in South Asian countries, the genetic diversity of circulating parasite populations is not well described. Other control measures which are traditionally effective against other Plasmodium parasites (e.g., P. falciparum) have proven to be less effective against P. vivax[5] due to its ability to form dormant liver-stage parasites[6]. These hypnozoites cause delayed blood-stage relapses, but can be cleared from the liver with primaquine or tafenoquine treatments, both regimens can cause severe haemolysis in individuals with G6PD deficiency[7]
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