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The V1016G mutation of the voltage-gated sodium channel (VGSC) gene contributes to the insecticide resistance of Aedes aegypti from Makassar, Indonesia

  • Arthropods and Medical Entomology - Original Paper
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Abstract

Aedes aegypti represents one of the main vectors of at least five relevant arthropod-borne viral infections in humans (i.e., Rift Valley fever, Dengue fever, Zika, chikungunya, and yellow fever) worldwide. Ae. aegypti control strategies are mostly based on using chemical insecticides (i.e., organophosphates, pyrethroids, carbamates, and organochlorines) and reducing larval sources. Furthermore, monitoring the growth activity and mapping the geographical distribution of insecticide resistance are mandatory, as recommended by the WHO. Accordingly, we conducted a study on the possible mechanism by which Ae. aegypti develops resistance to several frequently used chemical insecticides (i.e., λ-cyhalothrin, bendiocarb, cyfluthrin, deltamethrin, malathion, and permethrin) in the city of Makassar, Sulawesi, Indonesia. The results showed the progression of resistance toward the examined insecticides in Ae. aegypti populations in Makassar. The mortality rate of Ae. aegypti was less than 90%, with the highest resistance recorded against 0.75% permethrin. The molecular evaluation of the voltage-gated sodium channel gene (VGSC) showed a significant correlation of the V1016G gene mutation in the tested 0.75% permethrin-resistant Ae. aegypti phenotypes. Nevertheless, the F1534C point mutation in the VGSC gene of Ae. aegypti did not show a significant correlation with the phenotype exhibiting insecticide resistance to 0.75% permethrin. These results indicate that Ae. aegypti mosquitoes in Makassar City have developed resistance against the frequently used insecticide permethrin, which might spread to less-populated regions of Sulawesi. Therefore, we call for further entomological monitoring of insecticide resistance not only on Sulawesi but also on other closely located islands of the Indonesian archipelago to delay the spread of Ae. aegypti insecticide resistance.

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Funding

This work was supported and financed by DIKTI (Direktorat Jenderal Pendidikan Tinggi Indonesia) with an INSINAS scheme grant to PHH.

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Correspondence to P. H. Hamid.

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Competing interest

PHH and VIN performed the experiments and analyzed the data. PHH, AG, AT, and CH coordinated and designed the work and wrote and revised the manuscript. The authors declare that they have no competing interest.

Ethical clearance of the experiment

No ethical clearance was issued regarding these experiments. F0 Ae. aegypti were used for all experiments; therefore, no blood feedings from animals were performed for the mosquitoes. Other experiments related to the placement of ovitraps do not give any hazardous risk to citizens since regular control and collection of the eggs were performed before the larva hatched. Permission was obtained from the citizens of the participating houses before ovitraps were placed.

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Section Editor: Una Ryan

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Hamid, P.H., Ninditya, V.I., Ghiffari, A. et al. The V1016G mutation of the voltage-gated sodium channel (VGSC) gene contributes to the insecticide resistance of Aedes aegypti from Makassar, Indonesia. Parasitol Res 119, 2075–2083 (2020). https://doi.org/10.1007/s00436-020-06720-5

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  • DOI: https://doi.org/10.1007/s00436-020-06720-5

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