Knockdown resistance (kdr) of the voltage-gated sodium channel gene of Aedes aegypti population in Denpasar, Bali, Indonesia

Abstract

Background Aedes aegypti is the main vector of several arthropod-borne viral infections in the tropics profoundly affecting humans, such as dengue fever (DF), West Nile (WN), chikungunya and more recently Zika. Eradication of Aedes still largely depends on insecticides, which is the most cost-effective strategy, and often inefficient due to resistance development in exposed Aedes populations. We here conducted a study of Ae. aegypti resistance towards several insecticides regularly used in the city of Denpasar, Bali, Indonesia.Methods Aedes aegypti egg samples were collected with ovitraps and thereafter hatched in the insectary of the Gadjah Mada University. The F0 generation was used for all bioassay-related experiments and knockdown resistance (kdr) assays.ResultsResults clearly showed resistance development of Ae. aegypti against tested insecticides. Mortalities of Ae. aegypti were less than 90% with highest resistance observed against 0.75% permethrin. Mosquitoes from the southern parts of Denpasar presented high level of resistance pattern in comparison to those from the western and northern parts of Denpasar. Kdr analysis of voltage-gated sodium channel (Vgsc) gene showed significant association to S989P and V1016G mutations linked to resistance phenotypes against 0.75% permethrin. Conversely, Ae. aegypti F1534C gene mutation did not result in any significant correlation to resistance development.ConclusionsPeriodically surveillance of insecticide resistances in Ae. aegypti mosquitoes will help local public health authorities to set better goals and allow proper evaluation of on-going mosquito control strategies. Initial detection of insecticide resistance will contribute to conduct proper actions in delaying mosquito resistance development such as insecticide rotation or combination of compounds in order to prolong chemical efficacy in combating Ae. aegypti vectors in Indonesia.

The F1534C voltage‐sensitive sodium channel mutation confers 7‐ to 16‐fold resistance to pyrethroid insecticides in Aedes aegypti

“…V410L has been detected in the Americas, and V1016I has been detected only in the Americas, Europe and Africa . In contrast, S989P has been found only in Asia . V1016G mutations have been found in Asia and the Americas .…”

“…In contrast, S989P has been found only in Asia . V1016G mutations have been found in Asia and the Americas . F1534C is widely distributed in pyrethroid resistant A. aegypti globally .…”

Molecular Resistance Status of Aedes aegypti to the Organophosphate and Pyrethroid Insecticides in Central Sulawesi and East Nusa Tenggara Provinces, Indonesia

“…DNA isolation products were then stored at -80 o C until further analysis. PCR identification was conducted using two different primer sets targeting amino acid of the Ace-1 gene and domain II of amino acid loci of the VGSC gene, as described previously by Kawada et al, 2016 andHamid, et al, 2017. To identify ACE-1 gene mutation, PCR amplifications were carried out in the final volume of 25μl where 5 μl DNA isolation product was used as a template.…”

“…The most common target site resistance mechanism is associated with mutations of a target protein at the voltage-gated sodium channel (VGSC) gene, which is the target of pyrethroid (PY) insecticide and point mutation at the acetylcholinesterase (AchE) gene that is the target of OP and carbamate insecticides. Currently, several point mutations of insecticide knockdown (kdr) have been identified to be associated with the occurrence of pyrethroid resistance of Aedes aegypti [21]. These mutations of VGSC gene were reported to play roles in pyrethroid resistance of Aedes aegypti, especially the mutations at domain II (V410L); domain III (G923V, L982W, S989P, I1011M, I1011V, V1016G, V1016I); and domain III (T1520I, F1534C, D1763Y) [17,[21][22][23][24][25].…”

“…Currently, several point mutations of insecticide knockdown (kdr) have been identified to be associated with the occurrence of pyrethroid resistance of Aedes aegypti [21]. These mutations of VGSC gene were reported to play roles in pyrethroid resistance of Aedes aegypti, especially the mutations at domain II (V410L); domain III (G923V, L982W, S989P, I1011M, I1011V, V1016G, V1016I); and domain III (T1520I, F1534C, D1763Y) [17,[21][22][23][24][25]. Aedes aegypti kdr mutations with high allele frequency have been detected in many countries, including, US, India, Malaysia, Brazil, Myanmar, Thailand, Mexico, and Indonesia [17,21,22,[26][27][28][29] Acetylcholinesterase (AChE) gene has been described as a key enzyme of the cholinergic system, by regulating the level of acetylcholine and terminating nerve impulses by catalyzing the hydrolisis of acetylcholine [30,31].…”