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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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) |
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Arctic medicine. Tropical medicine RC955-962 Public aspects of medicine RA1-1270 |
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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 |
work_keys_str_mv |
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