Mutations Linked to Insecticide Resistance Not Detected in the or Genes in from Multiple Localities in Amazonian Brazil and Peru.

Indoor residual spray (IRS), mainly employing pyrethroid insecticides, is the most common intervention for preventing malaria transmission in many regions of Latin America; the use of long-lasting insecticidal nets (LLINs) has been more limited. Knockdown resistance () is a well-characterized target-site resistance mechanism associated with pyrethroid and DDT resistance. Most mutations detected in acetylcholinesterase-1 () and voltage-gated sodium channel () genes are non-synonymous, resulting in a change in amino acid, leading to the non-binding of the insecticide. In the present study, we analyzed target-site resistance in , the primary malaria vector in the Amazon, in multiple malaria endemic localities. We screened 988 wild-caught specimens of from three localities in Amazonian Peru and four in Amazonian Brazil. Collections were conducted between 2014 and 2021. The criteria were Amazonian localities with a recent history as malaria hotspots, primary transmission by , and the use of both IRS and LLINs as interventions. Fragments of (456 bp) and (228 bp) were amplified, sequenced, and aligned with sequences available in GenBank. We detected only synonymous mutations in the frequently reported codon 280 known to confer resistance to organophosphates and carbamates, but detected three non-synonymous mutations in other regions of the gene. Similarly, no mutations linked to insecticide resistance were detected in the frequently reported codon (995) at the S6 segment of domain II of . The lack of genotypic detection of insecticide resistance mutations by sequencing the and genes from multiple populations in Brazil and Peru could be associated with low-intensity resistance, or possibly the main resistance mechanism is metabolic.