Tristan P. W. Dennis, Jihad Eltaher Sulieman, Mujahid Nouredayem, Temesgen Ashine, Yehenew Ebstie, Adane Eyasu, Eba Alemayehu Simma, Endalew Zemene, Nigatu Negash, Abena Yigeremu, Muluken Assefa, Hamza Elzack, Alemayehu Dagne, Biniam Lukas, Mikiyas Gebremichael Bulto, Michaël C. Fontaine, Loïc Talignani, Ahmadali Enayati, Fatemeh Nikpoor, Ashwaq M. Al-Nazawi, Mohammed H. Al-Zahrani, Bouh Abdi Khaireh, Samatar Guelleh, Abdoul-Ilah Ahmed Abdi, Richard Allan, Seline Omondi, Bernard Abong’o, Sylvia Milanoi, Eric Ochomo, Ayman Ahmed, Jeanne N. Samake, John E. Gimnig, Cristina Rafferty, Faisal Ashraf, Patricia Pignatell, Marion Morris, Sanjay C. Nagi, Eric R. Lucas, Anastasia Hernández-Koutoucheva, Chris S. Clarkson, Patricia Doumbe-Belisse, Adrienne Epstein, Rebecca Brown, Anne L. Wilson, Alison M. Reynolds, Ellie Sherrard-Smith, Delenasaw Yewhalaw, Endalamaw Gadisa, Elfatih M Malik, Hmooda Toto Kafy, Martin J. Donnelly, David Weetman
The invasive urban malaria vector Anopheles stephensi threatens 126 million city dwellers in Africa. Controlling An. stephensi requires greater understanding of its origin, invasion dynamics, and insecticide resistance mechanisms. Analysis of 645 whole genomes sampled across Africa, the Middle East, and Asia supports an invasion scenario in which an initial South Asian introduction established a bridgehead population in Djibouti, which seeded distinct invasion fronts in Sudan, Ethiopia/Kenya, and Yemen. These incursions show contrasting rates and routes of spread shaped by landscape topology. Insecticide resistance is predominantly mediated by metabolic detoxification genes, with resistance haplotypes and copy-number amplifications introduced from South Asia. These findings, alongside a companion genomic resource, enable genomic surveillance of An. stephensi spread and resistance to aid control strategies.