ArticlePLoS computational biology2025
Effects of recombination on multi-drug resistance evolution in Plasmodium falciparum malaria.
Article in PLoS computational biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 3 of them syntheses that pooled it.
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Who cites it
7 citing papers in PubMed, 3 syntheses or guidelines pooled it.
- Spatio-temporal trends of the prevalence of Plasmodium falciparum antimalarial drug resistance markers across sub-Saharan Africa from 2010 to 2024: a systematic review and meta-analysis.BMC infectious diseases · 2026Pooled it
- Incidence of kelch13 and Pfmdr1 gene mutations associated with antimalarial drug resistance in Plasmodium falciparum isolates from Ethiopia: a systematic review and meta-analysis.BMC infectious diseases · 2026Pooled it
- A systematic review of epidemiological models for malaria transmission in Sub-Saharan Africa.Malaria journal · 2026Pooled it
- Slowing the spread of treatment failure to artemisinin-based combination therapies in Uganda.Nature communications · 2026Article
- Spatial and temporal description of antimalarial drug resistance markers in Ghana using targeted amplicon deep sequencing.Antimicrobial agents and chemotherapy · 2026Article
- The evolution of mosquito baiting: from chemical and electronic methods toward AI.Parasites & vectors · 2026Review
- Genetic Diversity and Allelic Distribution ofJournal of parasitology research · 2026Article
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Authors and funding
10 authors.
Funding
Abstract
When multiple beneficial alleles at multiple loci are present in a population but not linked together in any one individual, there is no general evolutionary result that determines whether recombination will speed up or slow down the emergence and evolution of genotypes carrying multiple beneficial alleles. Translated to infectious disease control, this evolutionary uncertainty means that when multiple types of drug resistance are present we do not know whether recombination will act more strongly to (1) bring together single-resistant genotypes into multi-drug resistant (MDR) genotypes, or (2) break apart MDR genotypes into single-resistant genotypes. In this paper, we introduce a new version of an established and validated individual-based malaria transmission model where we have added 25 drug-resistance related loci, individual mosquito bites, and mosquitoes feeding on multiple hosts in a single meal (interrupted feeds) allowing for recombination events of different Plasmodium falciparum genotypes from different hosts. Recombination among P. falciparum genotypes in this model occurs from two sources of variation, multi-clonal infections in single hosts and interrupted feeds on multiple hosts, and we show that 80% to 97% of MDR recombinant falciparum genotypes are projected to occur from single uninterrupted bites on hosts with multi-clonal infections (for malaria prevalence > 5%). Increases in the model's interrupted feeding rate slowly increase the number of recombination events occurring from interrupted feeds. A comparison of drug-resistance management strategies with this new model shows that, over a 15-year timeframe, triple artemisinin-combination therapies (ACT) strategies show the largest reductions in treatment failures and the longest delays until artemisinin resistance reaches a critical 1% threshold. Multiple first-line therapies (MFT) are second best under these criteria, and ACT cycling approaches are third best. When compared to cycling strategies, MFT strategies generate a greater diversity of recombinant genotypes but fewer recombination events generating MDR and slower emergence of these recombinant MDR genotypes.
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