Sodium channel activation underlies transfluthrin repellency in Aedes aegypti.

Journal Article (Journal Article)

Background

Volatile pyrethroid insecticides, such as transfluthrin, have received increasing attention for their potent repellent activities in recent years for controlling human disease vectors. It has been long understood that pyrethroids kill insects by promoting activation and inhibiting inactivation of voltage-gated sodium channels. However, the mechanism of pyrethroid repellency remains poorly understood and controversial.

Methodology/principal findings

Here, we show that transfluthrin repels Aedes aegypti in a hand-in-cage assay at nonlethal concentrations as low as 1 ppm. Contrary to a previous report, transfluthrin does not elicit any electroantennogram (EAG) responses, indicating that it does not activate olfactory receptor neurons (ORNs). The 1S-cis isomer of transfluthrin, which does not activate sodium channels, does not elicit repellency. Mutations in the sodium channel gene that reduce the potency of transfluthrin on sodium channels decrease transfluthrin repellency but do not affect repellency by DEET. Furthermore, transfluthrin enhances DEET repellency.

Conclusions/significance

These results provide a surprising example that sodium channel activation alone is sufficient to potently repel mosquitoes. Our findings of sodium channel activation as the principal mechanism of transfluthrin repellency and potentiation of DEET repellency have broad implications in future development of a new generation of dual-target repellent formulations to more effectively repel a variety of human disease vectors.

Full Text

Duke Authors

Cited Authors

  • Andreazza, F; Valbon, WR; Wang, Q; Liu, F; Xu, P; Bandason, E; Chen, M; Wu, S; Smith, LB; Scott, JG; Jiang, Y; Jiang, D; Zhang, A; Oliveira, EE; Dong, K

Published Date

  • July 8, 2021

Published In

Volume / Issue

  • 15 / 7

Start / End Page

  • e0009546 -

PubMed ID

  • 34237076

Pubmed Central ID

  • PMC8266078

Electronic International Standard Serial Number (EISSN)

  • 1935-2735

International Standard Serial Number (ISSN)

  • 1935-2727

Digital Object Identifier (DOI)

  • 10.1371/journal.pntd.0009546

Language

  • eng