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The origin, history, and resistance architecture of an invasive urban malaria mosquito in Africa.

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Title: The origin, history, and resistance architecture of an invasive urban malaria mosquito in Africa.
Authors: Dennis, Tristan P. W. (AUTHOR), Sulieman, Jihad Eltaher (AUTHOR), Nouredayem, Mujahid (AUTHOR), Ashine, Temesgen (AUTHOR), Ebstie, Yehenew (AUTHOR), Eyasu, Adane (AUTHOR), Simma, Eba A. (AUTHOR), Zemene, Endalew (AUTHOR), Negash, Nigatu (AUTHOR), Yigeremu, Abena (AUTHOR), Assefa, Muluken (AUTHOR), Elzack, Hamza (AUTHOR), Dagne, Alemayehu (AUTHOR), Lukas, Biniam (AUTHOR), Bulto, Mikiyas Gebremichael (AUTHOR), Fontaine, Michael C. (AUTHOR), Talignani, Loïc (AUTHOR), Enayati, Ahmadali (AUTHOR), Nikpoor, Fatemeh (AUTHOR), Al-Nazawi, Ashwaq M. (AUTHOR)
Source: Science. 7/9/2026, Vol. 393 Issue 6807, p1-14. 14p.
Subjects: Anopheles stephensi, Insecticide resistance, Malaria, Genetic epidemiology, Sudan (Region), Population genetics, Introduced species
Geographic Terms: Sudan, Asia, Pakistan, Middle East, South Asia, Horn of Africa, India, Africa, East Africa, Ethiopia, Djibouti
Abstract: 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. Editor's summary: The invasion of the malaria vector mosquito Anopheles stephensi into Africa has raised alarms because of its urban preference. Traditionally worse in rural areas, increased urban malarial exposure threatens to undo public health efforts to control the disease. To determine the origins of An. stephensi and its insecticide resistance, Dennis et al. sequenced 645 individual mosquitoes across the Horn of Africa and Yemen, as well as across its native range, the Middle East and South Asia. Their results suggest that a lineage closest to Afghanistan and Pakistan populations entered through the port of Djibouti and subsequently dispersed. Insecticide resistance is likely mediated through increased gene copy number rather than single mutations, which is important knowledge for efforts to control An. stephensi populations. —Corinne Simonti INTRODUCTION: In 2024, malaria resulted in more than 250 million cases and 550,000 deaths in Africa. Rural areas are typically most affected, especially during rainy seasons that provide abundant breeding sites for Anopheles mosquito vectors. First detected in Djibouti City in 2012, the invasion of Africa by the Asian malaria mosquito Anopheles stephensi has the potential to change the spatial and temporal distribution of malaria in Africa, undermining decades of malaria control progress. An. stephensi thrives in urban environments, where its populations are often less restricted by dry seasons. Now detected across the Horn of Africa, Kenya, and Yemen, and with sporadic reports in West Africa, An. stephensi has been associated with surges in malaria in Djibouti and Ethiopia, and modeling indicates an elevated threat to 126 million city dwellers across Africa. Control methods targeting native African Anopheles vectors appear poorly suited to An. stephensi, owing to variant population dynamics and behavior, as well as widespread insecticide resistance. RATIONALE: The origin and number of invasion events by An. stephensi into Africa and routes of subsequent expansion are currently unknown, with previous genetic sampling unable to discriminate among competing hypotheses. Additionally, resistance mechanisms in the invasive range do not appear to involve common and readily detected mutations in insecticide target sites. Genome-wide data are needed to reconstruct invasion routes, population structure, demographic history, and introduction timing, as well as the genomic architecture of insecticide resistance. RESULTS: Genome sequencing of 645 An. stephensi samples from the invasive range in East Africa and the native range in Asia and the Middle East reveals that invasive An. stephensi are most closely related to samples from Afghanistan and Pakistan. Three distinct invasion fronts—Sudan, Ethiopia-Kenya, and Yemen—predominantly derive from the same initially introduced population, with Djibouti the likely primary bridgehead. Sudanese and Ethiopian-Kenyan incursions show signs of isolation by distance, with diversity declining with distance from Port Sudan and Port of Djibouti respectively, which is consistent with serial founder events and stepwise spread after maritime introduction. Population size reconstructions show bottlenecks that are broadly consistent with discovery dates. Landscape genetic analysis identifies the Ethiopian Highlands as a major barrier to gene flow, explaining slower and more restricted spread in Ethiopia-Kenya compared with rapid homogeneous spread across Sudan's flatter terrain. Selection scans and haplotype clustering reveal strong selection at detoxification gene families across both native and invasive ranges. Extensive and uniform copy-number variation (CNV) in the invasive range, as well as haplotype sharing, indicate that resistance was introduced from Asia rather than evolving independently in Africa and that resistance is primarily determined by increased gene copy numbers rather than mutations. CONCLUSION: The An. stephensi invasion originated in Asia, most likely in coastal Pakistan or northern India through maritime introduction in Djibouti. This seeded subsequent invasions, which is consistent with the history of discovery. The open Sahel west of Sudan is a high-risk corridor for ongoing expansion, and whether detections in West Africa represent contiguous spread is an urgent question. An accompanying data and analytical toolkit, released by the MalariaGEN consortium, will support real-time genomic surveillance, monitoring, and intervention design across the invasive range. The invasion of Africa by An. stephensi.: Whole-genome sequence analysis revealed that invasive An. stephensi likely originated in South Asia. The initial bridgehead population in Djibouti seeded incursions into Sudan, Yemen, and through Ethiopia across the Horn of Africa and into Kenya. Contrasting rates of spread in Sudan and Ethiopia are underlain by different landscape types. Insecticide resistance in invasive populations is conferred by CNV at detoxification resistance genes, introduced from Asia. [ABSTRACT FROM AUTHOR]
Copyright of Science is the property of American Association for the Advancement of Science and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: The origin, history, and resistance architecture of an invasive urban malaria mosquito in Africa.
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– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: 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. Editor's summary: The invasion of the malaria vector mosquito Anopheles stephensi into Africa has raised alarms because of its urban preference. Traditionally worse in rural areas, increased urban malarial exposure threatens to undo public health efforts to control the disease. To determine the origins of An. stephensi and its insecticide resistance, Dennis et al. sequenced 645 individual mosquitoes across the Horn of Africa and Yemen, as well as across its native range, the Middle East and South Asia. Their results suggest that a lineage closest to Afghanistan and Pakistan populations entered through the port of Djibouti and subsequently dispersed. Insecticide resistance is likely mediated through increased gene copy number rather than single mutations, which is important knowledge for efforts to control An. stephensi populations. —Corinne Simonti INTRODUCTION: In 2024, malaria resulted in more than 250 million cases and 550,000 deaths in Africa. Rural areas are typically most affected, especially during rainy seasons that provide abundant breeding sites for Anopheles mosquito vectors. First detected in Djibouti City in 2012, the invasion of Africa by the Asian malaria mosquito Anopheles stephensi has the potential to change the spatial and temporal distribution of malaria in Africa, undermining decades of malaria control progress. An. stephensi thrives in urban environments, where its populations are often less restricted by dry seasons. Now detected across the Horn of Africa, Kenya, and Yemen, and with sporadic reports in West Africa, An. stephensi has been associated with surges in malaria in Djibouti and Ethiopia, and modeling indicates an elevated threat to 126 million city dwellers across Africa. Control methods targeting native African Anopheles vectors appear poorly suited to An. stephensi, owing to variant population dynamics and behavior, as well as widespread insecticide resistance. RATIONALE: The origin and number of invasion events by An. stephensi into Africa and routes of subsequent expansion are currently unknown, with previous genetic sampling unable to discriminate among competing hypotheses. Additionally, resistance mechanisms in the invasive range do not appear to involve common and readily detected mutations in insecticide target sites. Genome-wide data are needed to reconstruct invasion routes, population structure, demographic history, and introduction timing, as well as the genomic architecture of insecticide resistance. RESULTS: Genome sequencing of 645 An. stephensi samples from the invasive range in East Africa and the native range in Asia and the Middle East reveals that invasive An. stephensi are most closely related to samples from Afghanistan and Pakistan. Three distinct invasion fronts—Sudan, Ethiopia-Kenya, and Yemen—predominantly derive from the same initially introduced population, with Djibouti the likely primary bridgehead. Sudanese and Ethiopian-Kenyan incursions show signs of isolation by distance, with diversity declining with distance from Port Sudan and Port of Djibouti respectively, which is consistent with serial founder events and stepwise spread after maritime introduction. Population size reconstructions show bottlenecks that are broadly consistent with discovery dates. Landscape genetic analysis identifies the Ethiopian Highlands as a major barrier to gene flow, explaining slower and more restricted spread in Ethiopia-Kenya compared with rapid homogeneous spread across Sudan's flatter terrain. Selection scans and haplotype clustering reveal strong selection at detoxification gene families across both native and invasive ranges. Extensive and uniform copy-number variation (CNV) in the invasive range, as well as haplotype sharing, indicate that resistance was introduced from Asia rather than evolving independently in Africa and that resistance is primarily determined by increased gene copy numbers rather than mutations. CONCLUSION: The An. stephensi invasion originated in Asia, most likely in coastal Pakistan or northern India through maritime introduction in Djibouti. This seeded subsequent invasions, which is consistent with the history of discovery. The open Sahel west of Sudan is a high-risk corridor for ongoing expansion, and whether detections in West Africa represent contiguous spread is an urgent question. An accompanying data and analytical toolkit, released by the MalariaGEN consortium, will support real-time genomic surveillance, monitoring, and intervention design across the invasive range. The invasion of Africa by An. stephensi.: Whole-genome sequence analysis revealed that invasive An. stephensi likely originated in South Asia. The initial bridgehead population in Djibouti seeded incursions into Sudan, Yemen, and through Ethiopia across the Horn of Africa and into Kenya. Contrasting rates of spread in Sudan and Ethiopia are underlain by different landscape types. Insecticide resistance in invasive populations is conferred by CNV at detoxification resistance genes, introduced from Asia. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
  Group: Ab
  Data: <i>Copyright of Science is the property of American Association for the Advancement of Science and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
PLink https://search.ebscohost.com/login.aspx?direct=true&site=eds-live&db=pbh&AN=195271072
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        Type: general
      – SubjectFull: Insecticide resistance
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