Analysis of the Knockdown Resistance Locus (kdr) in Anopheles stephensi, An. arabiensis, and Culex pipiens s.l. for Insight Into the Evolution of Target-site Pyrethroid Resistance in Eastern Ethiopia

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  • 1 Department of Biology, Baylor University, Waco, Texas;
  • | 2 Department of Zoological Sciences, Addis Ababa University, Addis Ababa, Ethiopia;
  • | 3 Department of Bioinformatics and Genomics, University of North Carolina at Charlotte, Charlotte, North Carolina;
  • | 4 Institute of Bioinformatics, University of Georgia, Athens, Georgia;
  • | 5 Department of Molecular Biology and Biochemistry, Pennsylvania State University, State College, Pennsylvania;
  • | 6 Department of Biology, Jigjiga University, Jigjiga, Ethiopia

The malaria vector, Anopheles stephensi, which is typically restricted to South Asia and the Middle East, was recently detected in the Horn of Africa. Addressing the spread of this vector could involve integrated vector control that considers the status of insecticide resistance of multiple vector species in the region. Previous reports indicate that the knockdown resistance mutations (kdr) in the voltage-gated sodium channel (vgsc) are absent in both pyrethroid-resistant and pyrethroid-sensitive An. stephensi in eastern Ethiopia; however, similar information about other vector species in the same areas is limited. In this study, kdr and the neighboring intron were analyzed in An. stephensi, An. arabiensis, and Culex pipiens s.l. collected between 2016 and 2017 to determine the evolutionary history of kdr in eastern Ethiopia. A sequence analysis revealed that all of Cx. pipiens s.l. (N = 42) and 71.6% of the An. arabiensis (N = 67) carried kdr L1014F, which is known to confer target-site pyrethroid resistance. Intronic variation was only observed in An. stephensi (six segregating sites, three haplotypes), which was previously shown to have no kdr mutations. In addition, no evidence of non-neutral evolutionary processes was detected at the An. stephensi kdr intron, thereby further supporting the target-site mechanism not being a major resistance mechanism in this An. stephensi population. Overall, these results show key differences in the evolution of target-site pyrethroid/dichlorodiphenyltrichloroethane resistance mutations in populations of vector species from the same region. Variations in insecticide resistance mechanism profiles between eastern Ethiopian mosquito vectors may lead to different responses to insecticides used in integrated vector control.

Author Notes

Address correspondence to Tamar E. Carter, Department of Biology, Baylor University, Waco, TX 76798-7344. E-mail: tamar_carter@baylor.edu

These authors contributed equally to this work.

Financial support: This study was financially supported by Jigjiga University. This project was also funded by Baylor University and the University of North Carolina at Charlotte Multicultural Postdoctoral Fellowship.

Authors’ addresses: Tarmar E. Carter, Baylor University College of Arts and Sciences, Biology, Waco, TX, E-mail: tamar_carter@baylor.edu. Araya Gebresilassie, Department of Zoological Sciences, Addis Ababa University, Addis Ababa, Ethiopia, E-mail: arayagh2006@yahoo.com. Shantoy Hansel, Callum Montgomery, Karen Lopez, and Daniel Janies, University of North Carolina at Charlotte, Department of Bioinformatics and Genomics, Charlotte, NC, E-mails: shansel@uncc.edu, cmontg24@uncc.edu, klopez1@uncc.edu, and djanies@uncc.edu. Lambodhar Damodaran, University of Georgia, Institute of Bioinformatics, Athens, GA, E-mail: lambodhar.damodaran@uga.edu. Victoria Bonnell, Pennsylvania State University Department of Biochemistry and Molecular Biology, Department of Molecular Biology and Biochemistry, Hershey, PA, E-mail: vab18@psu.edu. Solomon Yared, Jigjiga University, Department of Biology, Jigjiga, Somali Region, Ethiopia, E-mail: solyar2005@yahoo.com.

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