Mitochondrial phylogeography and insecticide resistance of Aedes aegypti in Kenya
- 1International Centre of Insect Physiology and Ecology, Nairobi, Kenya
- 2Department of Genetics, University of Cambridge, Cambridge, United Kingdom
- 3Cambridge Biosecurity Hub, Cambridge, United Kingdom
Abstract
Aedes aegypti is the primary vector of arboviruses such as dengue, yellow fever, Zika, and chikungunya. Here, we investigate the mitochondrial DNA (mtDNA) structure and insecticide resistance of Ae. aegypti populations across Kenya. Using 175 newly sequenced Kenyan COI mtDNA fragments, along with global reference sequences, we assess maternal ancestry and phylogeographic structure. Genetic structure across Kenya was not well explained by isolation-by-distance alone, with several populations deviating from this pattern. Nairobi and Mombasa, separated by >400 km, showed greater maternal genetic similarity than expected under isolation-by-distance, a pattern that may reflect gene flow along transportation corridors. Conversely, Ukunda, around 30 km from Mombasa, was comparatively divergent, and populations in Western Kenya were genetically distinct. We found no evidence of non-African ancestry in mtDNA from Rabai or Mombasa despite its previous detection in the nuclear genomes of these populations. Instead, a subset of samples from Marigat and Ukunda showed the closest maternal affinity to West African and non-African lineages. Insecticide assays revealed high susceptibility to bendiocarb, deltamethrin, and fenitrothion across populations, but substantial resistance to permethrin, particularly at coastal sites. Genotyping of the kdr 1534C allele showed the highest resistance allele frequencies in coastal populations, broadly consistent with the phenotypic patterns. This variation in resistance was not associated with mitochondrial ancestry, suggesting that local selection pressures rather than shared maternal ancestry may be shaping resistance. Together, these findings describe the maternal genetic structure of Ae. aegypti in Kenya and show that localised resistance evolution, in the absence of organised Ae. aegypti-targeted control, underscores the need to monitor resistance mechanisms. Author summary: Aedes aegypti mosquitoes transmit devastating viral diseases including dengue, yellow fever, Zika, and chikungunya to billions of people worldwide. Understanding the genetic makeup and insecticide resistance patterns of these mosquitoes in their ancestral African range is crucial for disease control. We studied Ae. aegypti populations across Kenya by analysing their mitochondrial DNA—genetic material inherited solely through the maternal line—and testing their susceptibility to commonly used insecticides. We discovered unexpected patterns of genetic relationships: mosquito populations in Nairobi and the coastal city of Mombasa, separated by over 400 kilometres, were genetically similar, likely due to mosquitoes travelling along major transport routes. Conversely, Ukunda, merely 30 kilometres from Mombasa, showed distinct genetic differences, possibly due to geographical barriers like water bodies. Intriguingly, whilst previous studies found evidence of non-African mosquitoes invading Kenya’s coast through nuclear DNA analysis, we found no such evidence in mitochondrial DNA, suggesting complex evolutionary processes at play. Our insecticide testing revealed concerning resistance to permethrin, particularly in coastal populations, despite the absence of organised mosquito control programmes targeting Ae. aegypti in Kenya. This resistance appears driven by local selection pressures rather than mosquito ancestry. These findings highlight the urgent need for resistance monitoring and inform strategies for controlling mosquito-borne diseases in East Africa, where dengue outbreaks increasingly threaten public health.
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BibTeX
@article{musimbi2026mitochondrial,
title = {{Mitochondrial phylogeography and insecticide resistance of Aedes aegypti in Kenya}},
author = {Brenda Musimbi and Sandy Hickson and Trizah K. Milugo and Eleanor Robinson-Rice and Josephine Osalla and Gilbert Rotich and Frank Jiggins and David P. Tchouassi},
journal = {PLOS Neglected Tropical Diseases},
year = {2026},
month = sep,
doi = {10.1371/journal.pntd.0014670},
url = {https://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0014670},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Mitochondrial phylogeography and insecticide resistance of Aedes aegypti in Kenya
AU - Brenda Musimbi
AU - Sandy Hickson
AU - Trizah K. Milugo
AU - Eleanor Robinson-Rice
AU - Josephine Osalla
AU - Gilbert Rotich
AU - Frank Jiggins
AU - David P. Tchouassi
PY - 2026
DA - 2026/09/08
JO - PLOS Neglected Tropical Diseases
DO - 10.1371/journal.pntd.0014670
UR - https://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0014670
AB - Aedes aegypti is the primary vector of arboviruses such as dengue, yellow fever, Zika, and chikungunya. Here, we investigate the mitochondrial DNA (mtDNA) structure and insecticide resistance of Ae. aegypti populations across Kenya. Using 175 newly sequenced Kenyan COI mtDNA fragments, along with global reference sequences, we assess maternal ancestry and phylogeographic structure. Genetic structure across Kenya was not well explained by isolation-by-distance alone, with several populations deviating from this pattern. Nairobi and Mombasa, separated by >400 km, showed greater maternal genetic similarity than expected under isolation-by-distance, a pattern that may reflect gene flow along transportation corridors. Conversely, Ukunda, around 30 km from Mombasa, was comparatively divergent, and populations in Western Kenya were genetically distinct. We found no evidence of non-African ancestry in mtDNA from Rabai or Mombasa despite its previous detection in the nuclear genomes of these populations. Instead, a subset of samples from Marigat and Ukunda showed the closest maternal affinity to West African and non-African lineages. Insecticide assays revealed high susceptibility to bendiocarb, deltamethrin, and fenitrothion across populations, but substantial resistance to permethrin, particularly at coastal sites. Genotyping of the kdr 1534C allele showed the highest resistance allele frequencies in coastal populations, broadly consistent with the phenotypic patterns. This variation in resistance was not associated with mitochondrial ancestry, suggesting that local selection pressures rather than shared maternal ancestry may be shaping resistance. Together, these findings describe the maternal genetic structure of Ae. aegypti in Kenya and show that localised resistance evolution, in the absence of organised Ae. aegypti-targeted control, underscores the need to monitor resistance mechanisms. Author summary: Aedes aegypti mosquitoes transmit devastating viral diseases including dengue, yellow fever, Zika, and chikungunya to billions of people worldwide. Understanding the genetic makeup and insecticide resistance patterns of these mosquitoes in their ancestral African range is crucial for disease control. We studied Ae. aegypti populations across Kenya by analysing their mitochondrial DNA—genetic material inherited solely through the maternal line—and testing their susceptibility to commonly used insecticides. We discovered unexpected patterns of genetic relationships: mosquito populations in Nairobi and the coastal city of Mombasa, separated by over 400 kilometres, were genetically similar, likely due to mosquitoes travelling along major transport routes. Conversely, Ukunda, merely 30 kilometres from Mombasa, showed distinct genetic differences, possibly due to geographical barriers like water bodies. Intriguingly, whilst previous studies found evidence of non-African mosquitoes invading Kenya’s coast through nuclear DNA analysis, we found no such evidence in mitochondrial DNA, suggesting complex evolutionary processes at play. Our insecticide testing revealed concerning resistance to permethrin, particularly in coastal populations, despite the absence of organised mosquito control programmes targeting Ae. aegypti in Kenya. This resistance appears driven by local selection pressures rather than mosquito ancestry. These findings highlight the urgent need for resistance monitoring and inform strategies for controlling mosquito-borne diseases in East Africa, where dengue outbreaks increasingly threaten public health.
SN - 1935-2735
ER -