Sodium channel activation underlies transfluthrin repellency in Aedes aegypti.

<h4>Background</h4>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 an...

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Autores principales: Felipe Andreazza, Wilson R Valbon, Qiang Wang, Feng Liu, Peng Xu, Elizabeth Bandason, Mengli Chen, Shaoying Wu, Leticia B Smith, Jeffrey G Scott, Youfa Jiang, Dingxin Jiang, Aijun Zhang, Eugenio E Oliveira, Ke Dong
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spelling oai:doaj.org-article:c5150aa6523148f9824aaa067bf3b1872021-12-02T20:23:47ZSodium channel activation underlies transfluthrin repellency in Aedes aegypti.1935-27271935-273510.1371/journal.pntd.0009546https://doaj.org/article/c5150aa6523148f9824aaa067bf3b1872021-07-01T00:00:00Zhttps://doi.org/10.1371/journal.pntd.0009546https://doaj.org/toc/1935-2727https://doaj.org/toc/1935-2735<h4>Background</h4>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.<h4>Methodology/principal findings</h4>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.<h4>Conclusions/significance</h4>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.Felipe AndreazzaWilson R ValbonQiang WangFeng LiuPeng XuElizabeth BandasonMengli ChenShaoying WuLeticia B SmithJeffrey G ScottYoufa JiangDingxin JiangAijun ZhangEugenio E OliveiraKe DongPublic Library of Science (PLoS)articleArctic medicine. Tropical medicineRC955-962Public aspects of medicineRA1-1270ENPLoS Neglected Tropical Diseases, Vol 15, Iss 7, p e0009546 (2021)
institution DOAJ
collection DOAJ
language EN
topic Arctic medicine. Tropical medicine
RC955-962
Public aspects of medicine
RA1-1270
spellingShingle Arctic medicine. Tropical medicine
RC955-962
Public aspects of medicine
RA1-1270
Felipe Andreazza
Wilson R Valbon
Qiang Wang
Feng Liu
Peng Xu
Elizabeth Bandason
Mengli Chen
Shaoying Wu
Leticia B Smith
Jeffrey G Scott
Youfa Jiang
Dingxin Jiang
Aijun Zhang
Eugenio E Oliveira
Ke Dong
Sodium channel activation underlies transfluthrin repellency in Aedes aegypti.
description <h4>Background</h4>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.<h4>Methodology/principal findings</h4>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.<h4>Conclusions/significance</h4>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.
format article
author Felipe Andreazza
Wilson R Valbon
Qiang Wang
Feng Liu
Peng Xu
Elizabeth Bandason
Mengli Chen
Shaoying Wu
Leticia B Smith
Jeffrey G Scott
Youfa Jiang
Dingxin Jiang
Aijun Zhang
Eugenio E Oliveira
Ke Dong
author_facet Felipe Andreazza
Wilson R Valbon
Qiang Wang
Feng Liu
Peng Xu
Elizabeth Bandason
Mengli Chen
Shaoying Wu
Leticia B Smith
Jeffrey G Scott
Youfa Jiang
Dingxin Jiang
Aijun Zhang
Eugenio E Oliveira
Ke Dong
author_sort Felipe Andreazza
title Sodium channel activation underlies transfluthrin repellency in Aedes aegypti.
title_short Sodium channel activation underlies transfluthrin repellency in Aedes aegypti.
title_full Sodium channel activation underlies transfluthrin repellency in Aedes aegypti.
title_fullStr Sodium channel activation underlies transfluthrin repellency in Aedes aegypti.
title_full_unstemmed Sodium channel activation underlies transfluthrin repellency in Aedes aegypti.
title_sort sodium channel activation underlies transfluthrin repellency in aedes aegypti.
publisher Public Library of Science (PLoS)
publishDate 2021
url https://doaj.org/article/c5150aa6523148f9824aaa067bf3b187
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