What question did this study set out to answer?

This research aimed to assess the genetic evolution of resistance and infection rates in Anopheles funestus across different Kenyan regions.

May 17, 2026Open Access

Signature of resistance gene evolution and pyrethroid resistance escalation in the major malaria vector Anopheles funestus across Kenyan malaria-endemic regions separated by the Rift Valley

Key Points

This research aimed to assess the genetic evolution of resistance and infection rates in Anopheles funestus across different Kenyan regions.
Genotyped Anopheles funestus populations using polymerase chain reaction (PCR) for resistance markers.
Screened for Plasmodium sporozoite infection using Taq Man assay and nested PCR.
Evaluated phenotypic resistance through diagnostic assays and piperonyl butoxide synergistic tests.
L119F-GSTe2 increased across regions, lowering odds of Plasmodium infection (OR 0.2, P=0.046).
4.3 kb allele showed higher infection rates (OR 5.7, P=0.049).
High pyrethroid resistance in KV, lower mortality in KV despite PBO exposure, and widespread DDT resistance with susceptibility to certain insecticides.

Abstract

Abstract Background Landscape features such as the Rift Valley (RV) can restrict gene flow in malaria vectors and influence resistance patterns. Here, we assessed Plasmodium infection rates, resistance alleles and profiles in Anopheles funestus s.s. populations across Kenyan malaria-endemic regions separated by the RV. Methods Anopheles funestus s.s. populations in western, coastal and Kerio Valley (KV, within the RV) were genotyped for key resistance markers using polymerase chain reaction (PCR). Taq Man assay combined with nested PCR were used to screen the samples for Plasmodium sporozoite infection and association with resistance alleles and genotype frequencies assessed using Fisher’s exact test or Pearson’s chi-square test. Following established WHO guidelines, phenotypic resistance using F1 progeny was also assessed using diagnostic, intensity and piperonyl butoxide (PBO)-synergistic assays. Results The 4.3kb-SV ( n = 336) and G454A-Cyp9k1 ( n = 445) alleles were nearly fixed in western Kenya but declined towards the RV and coast, whereas L119F-GSTe2 ( n = 392) increased across a west-KV-coast gradient with a novel haplotype distinct from known African variants detected at the coast. There were lower odds of Plasmodium infection in mosquitoes with L119F-GSTe2-RR than RS genotype ( OR 0.2, P = 0.046). Likewise, mosquitoes harboring the R allele of the 4.3 kb marker had higher Plasmodium infection rates than the S allele ( OR 5.7, P = 0.049). An. funestus populations exhibited a high degree of pyrethroid resistance with intensity higher in KV compared to western Kenya, a traditional malaria hotspot. Pre-exposure to PBO increased mortality for type II (deltamethrin, alpha-cypermethrin), than I (permethrin) pyrethroids, yet mortality remained lower in KV, suggesting non-P450-mediated resistance. An. funestus mosquitoes from the coast showed extreme permethrin resistance (< 10% mortality at 10 × dose). Resistance to dichlorodiphenyltrichloroethane was widespread, while all populations remained fully susceptible to bendiocarb, pirimiphos-methyl, clothianidin, and chlorfenapyr. Conclusions Region-specific selection may drive varying resistance profiles in An. funestus across Kenyan malaria-endemic regions separated by the Rift Valley, with implications for malaria transmission and insecticide resistance management.

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