First report of V1016G and S989P knockdown resistant (kdr) mutations in pyrethroid-resistant Sri Lankan Aedes aegypti mosquitoes

Abstract

BackgroundDengue is a serious arboviral disease in Sri Lanka with a large number of dengue fever (DF) cases every year. Control of the primary vector Aedes aegypti depends upon larval habitat source reduction and insecticide application. However, increases in the number of reported cases suggest the inefficiency of current control strategies and the possibility of resistance to currently used insecticides. Early detection of mutations in the voltage-gated sodium channel (vgsc) gene that confer knockdown resistance (kdr) to pyrethroid insecticides is important in resistance management in vector populations.ResultsResistance to pyrethroid insecticides was detected in the three populations studied. Polymerase chain reaction was used to detect the presence of two kdr mutations F1534C and V1016G. During this process a S989P mutation was also detected in pyrethroid-resistant Ae. aegypti populations. These mutations were found to be widespread and frequent in the collections studied.ConclusionsTo our knowledge, this study reveals for the first time the presence of V1016G and S989P mutant alleles in the vgsc of Sri Lankan Ae. aegypti populations. The spread of the mutant alleles throughout the country poses a threat of increased resistance to pyrethroids. Long-term insecticide applications and indiscriminate use of pyrethroids has led to the evolution of resistance. More strategic and diverse strategies, including novel insecticides with new modes of action and community participation, should be engaged for Ae. aegypti control.Electronic supplementary materialThe online version of this article (10.1186/s13071-018-3113-0) contains supplementary material, which is available to authorized users.

Distribution and pyrethroid resistance status of Aedes aegypti and Aedes albopictus populations and possible phylogenetic reasons for the recent invasion of Aedes aegypti in Nepal

“…aegypti populations in Thailand, in which mosquitoes of the wild type 1016V were homozygous for the F1534C mutation, 1016 heterozygous (1016V and V1016G) mosquitoes were 1534 heterozygous (1534F and F1534C), and mosquitoes with homozygous V1016G mutations were homozygous for the wild type 1534F. In Thailand, the frequency of the F1534C mutation is considerably more common than that of the V1016G mutation [34,36,42], a pattern which has also been reported in Vietnam [43] and Sri Lanka [50]. On the contrary, we found that the V1016G mutation was more common relative to the F1534C mutation.…”

Evolution of kdr haplotypes in worldwide populations of Aedes aegypti: Independent origins of the F1534C kdr mutation

“…This is consistent with 1534C having more than one origin. Likewise, in Sri Lanka although the triple mutant genotype was found, no individual was homozygote for the three mutations [42].…”

Identifying the fitness costs of a pyrethroid-resistant genotype in the major arboviral vector Aedes aegypti

“…F1534C is a phenylalanine to cysteine substitution at position 1534 in domain III, segment 6 [11]. The V1016G kdr mutation is widely distributed across Asian A. aegypti populations [15,16] and has also recently been documented in Aedes albopictus [17,18]. Alone, or in combination with other mutations such as F1534C [13,17,18], these alleles confer significant protection against pyrethroid insecticides [11].…”