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Temporal Pattern of Mutations in the Knockdown Resistance (kdr) Gene of Aedes aegypti Mosquitoes Sampled from Southern Taiwan

Sandrine BidudaDepartment of Immunology and Microbiology, Centre for Medical Parasitology, University of Copenhagen, Copenhagen, Denmark;
Department of Infectious Diseases, Copenhagen University Hospital, Copenhagen, Denmark;

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Chia-Hsien LinDepartment of Public Health, Global Health Section, University of Copenhagen, Copenhagen, Denmark;

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Fatma SalehDepartment of Allied Health Sciences, School of Health and Medical Sciences, The State University of Zanzibar, Zanzibar, Tanzania

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Flemming KonradsenDepartment of Public Health, Global Health Section, University of Copenhagen, Copenhagen, Denmark;

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Helle HanssonDepartment of Immunology and Microbiology, Centre for Medical Parasitology, University of Copenhagen, Copenhagen, Denmark;
Department of Infectious Diseases, Copenhagen University Hospital, Copenhagen, Denmark;

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Karin L. SchiølerDepartment of Public Health, Global Health Section, University of Copenhagen, Copenhagen, Denmark;

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Michael AlifrangisDepartment of Immunology and Microbiology, Centre for Medical Parasitology, University of Copenhagen, Copenhagen, Denmark;
Department of Infectious Diseases, Copenhagen University Hospital, Copenhagen, Denmark;

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Aedes mosquitoes are the principal dengue vector in Taiwan, where the use of insecticides is a key element in the national control strategy. However, control efforts are constrained by the development of resistance to most insecticides, including pyrethroids. In this study, mutations in the voltage-gated sodium channel (VGSC) gene resulting in knockdown resistance (kdr) were examined in Aedes aegypti. Fragments of the VGSC gene were polymerase chain reaction (PCR)-amplified followed by restriction fragment length polymorphism analysis in samples from various settings in Southern Taiwan covering dry and wet seasons from 2013 to 2015. Three kdr mutations were identified: V1023G, D1794Y, and F1534C, with observed frequencies of 0.36, 0.55, and 0.33, respectively, in the dry season of 2013–2014. Exploring for temporal changes, the most important observation was the 1534C allele frequency increment in the following season to 0.60 (P < 0.05). This study suggests that continued insecticide pressure is driving the mutational changes, although the selection is ambiguous in the mosquito population.

Author Notes

Address correspondence to Sandrine Biduda or Michael Alifrangis, Centre for Medical Parasitology, University of Copenhagen, Bartolinsgade 2, CSS, Bldg. 22–23, Copenhagen K 1014, Denmark. E-mails: sandrine@sund.ku.dk or micali@sund.ku.dk

Financial support: This study was supported by the University of Copenhagen.

Authors’ addresses: Sandrine Biduda, Helle Hansson, and Michael Alifrangis, Center for Medical Parasitology, University of Copenhagen, Copenhagen, Denmark, E-mails: sandrine@sund.ku.dk, hellehan@sund.ku.dk, and micali@sund.ku.dk. Chia-Hsien Lin, Karin Linda Schiøler, and Flemming Konradsen, Department of Public Health, School of Global Health, University of Copenhagen, Copenhagen, Denmark, E-mails: chlin@sund.ku.dk, ksch@sund.ku.dk, and flko@sund.ku.dk. Fatma Saleh, Department of Allied Health Sciences, School of Health and Medical Sciences, The State University of Zanzibar, Zanzibar, Tanzania, E-mail: fatmahamidsaleh@gmail.com.

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