ArticleNature communications2024
Population genomics and transcriptomics of Plasmodium falciparum in Cambodia and Vietnam uncover key components of the artemisinin resistance genetic background.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed.
- Experimental evolution and functional genetics identify KIC1 as a determinant of reduced artemisinin susceptibility in BangladeshibioRxiv : the preprint server for biology · 2026Article
- Global-scale population genetic analysis of Plasmodium falciparum identifies region-specific patterns of malaria parasite adaptation.Nature communications · 2026Article
- Application Strategy and Research Progress of Large-Scale Population Drug Intervention in Malaria Control.Tropical medicine and infectious disease · 2026Review
- A Fe-incorporated bioreactor platform exhibiting antimalarial activity and enhanced response to artemisinin.Antimicrobial agents and chemotherapy · 2026Article
- Integrative genomics ofbioRxiv : the preprint server for biology · 2026Article
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- Mapping the global distribution and spread of theVirus evolution · 2026Article
- Metabolic engineering and late-stage functionalization expand the chemical space of the antimalarial premarineosin A.Communications chemistry · 2025Article
- Low-volumeMicrobial genomics · 2025Article
- Review
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25 authors.
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Abstract
The emergence of Plasmodium falciparum parasites resistant to artemisinins compromises the efficacy of Artemisinin Combination Therapies (ACTs), the global first-line malaria treatment. Artemisinin resistance is a complex genetic trait in which nonsynonymous SNPs in PfK13 cooperate with other genetic variations. Here, we present population genomic/transcriptomic analyses of P. falciparum collected from patients with uncomplicated malaria in Cambodia and Vietnam between 2018 and 2020. Besides the PfK13 SNPs, several polymorphisms, including nonsynonymous SNPs (N1131I and N821K) in PfRad5 and an intronic SNP in PfWD11 (WD40 repeat-containing protein on chromosome 11), appear to be associated with artemisinin resistance, possibly as new markers. There is also a defined set of genes whose steady-state levels of mRNA and/or splice variants or antisense transcripts correlate with artemisinin resistance at the base level. In vivo transcriptional responses to artemisinins indicate the resistant parasite's capacity to decelerate its intraerythrocytic developmental cycle (IDC), which can contribute to the resistant phenotype. During this response, PfRAD5 and PfWD11 upregulate their respective alternatively/aberrantly spliced isoforms, suggesting their contribution to the protective response to artemisinins. PfRAD5 and PfWD11 appear under selective pressure in the Greater Mekong Sub-region over the last decade, suggesting their role in the genetic background of the artemisinin resistance.
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