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The evolution of genetic mechanisms for host immune evasion and anti-malarial resistance has enabled the  Plasmodium falciparum  malaria parasite to inflict high morbidity and mortality on human populations. Most studies of  P. falciparum  genetic diversity have focused on single-nucleotide polymorphisms (SNPs), assisting the identification of drug resistance-associated loci such as the chloroquine related  crt  and sulfadoxine-pyrimethamine related  dhfr . Whilst larger structural variants are known to impact adaptation, for example,  mdr1  duplications with anti-malarial resistance, no large-scale, genome-wide study on clinical isolates has been undertaken using whole genome sequencing data. By applying a structural variant detection pipeline across whole genome sequence data from 2,855 clinical isolates in 21 malaria-endemic countries, we identified >70,000 specific deletions and >600 duplications. Most structural variants are rare (48.5% of deletions and 94.7% of duplications are found in single isolates) with 2.4% of deletions and 0.2% of duplications found in >5% of global isolates. A subset of variants was present at high frequency in drug-resistance related genes including  mdr1 , the  gch1  promoter region, and a putative novel duplication of  crt . Regional-specific variants were identified, and a companion visualisation tool has been developed to assist web-based investigation of these polymorphisms by the wider scientific community.

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An analysis of large structural variation in global Plasmodium falciparum isolates identifies a novel duplication of the chloroquine resistance associated gene