Loss of pyrethroid resistance in newly established laboratory colonies of Aedes aegypti

Abstract

BackgroundResistance to pyrethroid insecticides in Aedes aegypti has become widespread after almost two decades of their frequent use to reduce arbovirus transmission. Despite this, use of pyrethroids continues because they are relatively inexpensive and because of their low human toxicity. Resistance management has been proposed as a means to retain the use of pyrethroids in natural populations. A key component of resistance management assumes that there is a negative fitness associated with resistance alleles so that when insecticides are removed, resistance alleles will decline in frequency. At least three studies in Ae. aegypti have demonstrated a decrease in pyrethroid resistance once the insecticide is removed.\n\nMethods/Principal FindingsThe present study aims to evaluate variation in the loss of pyrethroid resistance among newly established laboratory populations of Ae. aegypti from Mexico. Eight field collections were maintained for up to eight generations and we recorded changes in the frequencies of mutations at the V1,016I locus and at the F1,534C locus in the voltage gated sodium channel (VGSC) gene. I1,016 and C1,534 confer resistance. We also examined resistance ratios (RR) with type 1 and 2 pyrethroids.\n\nConclusions/SignificanceWe demonstrate that, in general, the frequency of the Ae. aegypti pyrethroid resistance alleles I1,016 and C1,534 decline when they are freed from pyrethroid pressure in the laboratory. However, the pattern of decline is strain dependent. In agreement with earlier studies, RR was positively correlated with I1,016 resistant allele frequencies and showed significant protection against permethrin, and deltamethrin whereas F1534C showed protection against permethrin but not against deltamethrin.\n\nAuthor SummaryThe author is interested in the evolution of genes that confer resistance to insecticides, especially when this evolution affects binding of insecticides to their target site. The Voltage Gated Sodium Channel gene represents an excellent opportunity to understand how mutations at the target site(s) affect the evolution of resistance in many different pest insect species including Aedes aegypti, the primary vector of Dengue Virus, Yellow Fever, Zika and Chikungunya arboviruses.