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The genetics of Plasmodium as an intracellular, mostly haploid, sexually reproducing, eukaryotic organism with a complex life cycle, presents unprecedented challenges in studying drug resistance. This article summarizes current knowledge on the genetic basis of artemisinin resistance (AR) – a main component of current drug therapies for falciparum malaria. Although centered on nonsynonymous single-nucleotide polymorphisms (nsSNPs), we describe multifaceted resistance mechanisms as part of a complex, cumulative genetic trait that involves regulation of expression by a wide array of polymorphisms in noncoding regions. These genetic variations alter transcriptome profiles linked to Plasmodium's development and population dynamics, ultimately influencing the emergence and spread of the resistance.

Original publication

DOI

10.1016/j.pt.2024.09.002

Type

Journal article

Journal

Trends in Parasitology

Publication Date

01/01/2024