Comparing Mitochondrial Gene Sequences of Aedes Aegypti in East Africa to the Global Anthropophilic Strain

Abstract

Advances in genotyping methods have shed more light into mosquito genetics and improved our understanding of vector-borne disease transmission cycles. Outside of Africa, Aedes aegypti, the main vector of arboviruses such as dengue, chikungunya, yellow fever, and Zika viruses, prefers humans for a blood meal, resting and breeding in close association with human settlements. However, in its native African ecology, both domestic (Aedes aegypti aegypti) and sylvatic (forest) (Aedes aegypti formosus) lineages occur. Further, the African Ae. aegypti populations have been found to exhibit divergence in typically conserved mitochondrial cytochrome c oxidase subunit I (COI) genes and traits of epidemiological importance, including developmental time, foraging, oviposition, and resting behaviour. This study tested the hypothesis that mitochondrial variation in Ae. aegypti populations correlates with dengue outbreak occurrence patterns. Specifically, molecular investigations were conducted on mitochondrial cytochrome coxidase subunits I and II (COI, COII), and cytochrome b (cyt b) gene sequences of Ae. aegypti generated by Sanger sequencing. Additional sequences were retrieved from GenBank and the Barcode of Life Data (BOLD) portal. The vectors were sampled from selected sites in Kenya viz: Kilifi and Kwale counties in coastal Kenya (endemic for dengue), Maasai Mara National Reserve in Narok County (sylvatic), and Kakamega, Bungoma, and Busia counties in western Kenya (non-dengue endemic region). The fragment sizes of the generated Ae. aegypti sequences were ~1100 bp, 700 bp, and ~350 bp for COI, COII, and cyt b, respectively. These sequences were analysed by maximum likelihood phylogenetic reconstruction. The COI gene sequences from sylvatic and domestic settings resolved Ae. aegypti into three lineages. The majority of the COI sequences of samples from Bungoma, Busia, and Kakamega counties clustered with referenced sylvatic rather than domestic strains, suggesting occurrence of the forest form in the domestic sites in these counties in Kenya. On the other hand, most COI sequences of samples from Kilifi, Narok, and Kwale counties clustered with referenced domestic than sylvatic strains. Since the domestic form is a better vector of dengue virus than the forest form, these findings, coupled with factors such as temperature and humidity, may explain recurrent dengue outbreaks at the coast of Kenya.