Evidence map›Paper›PMID 33559956›Full record

ArticlePest management science2021

A first, naturally occurring substitution at the second pyrethroid receptor of voltage-gated sodium channel of Aedes aegypti.

Kentaro Itokawa, Shogo Furutani, Aki Takaoka, Yoshihide Maekawa, Kyoko Sawabe, Osamu Komagata, Takashi Tomita, José Luiz de Lima Filho, Luiz Carlos Alves, Shinji Kasai

Open access · hybridAbstract read
In one paragraph

Article in Pest management science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.5field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 24 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 4 countries.

Kentaro Itokawa *Pathogen Genomics Center, National Institute of Infectious Diseases, Tokyo, Japan.ORCID https://orcid.org/0000-0003-1300-9883
Shogo Furutani *Department of Medical Entomology, National Institute of Infectious Diseases, Tokyo, Japan.
Aki TakaokaDepartment of Medical Entomology, National Institute of Infectious Diseases, Tokyo, Japan.
Yoshihide MaekawaDepartment of Medical Entomology, National Institute of Infectious Diseases, Tokyo, Japan.
Kyoko SawabeDepartment of Medical Entomology, National Institute of Infectious Diseases, Tokyo, Japan.
Osamu KomagataDepartment of Medical Entomology, National Institute of Infectious Diseases, Tokyo, Japan.
Takashi TomitaDepartment of Medical Entomology, National Institute of Infectious Diseases, Tokyo, Japan.
José Luiz de Lima FilhoLaboratório de Imunopatologia Keizo Asami, Universidade Federal de Pernambuco, Recife, Brazil.
Luiz Carlos AlvesLaboratório de Imunopatologia Keizo Asami, Universidade Federal de Pernambuco, Recife, Brazil.
Shinji KasaiDepartment of Medical Entomology, National Institute of Infectious Diseases, Tokyo, Japan.ORCID https://orcid.org/0000-0002-3837-6551
National Institute of Infectious Diseases · JPUniversidade Federal de Pernambuco · BR

Funding

Japan Agency for Medical Research and DevelopmentMinistry of Education, Culture, Sports, Science and Technology
6 · The paper itself

Abstract

backgroundAedes aegypti is a remarkably effective mosquito vector of epidemiologically important arboviral diseases including dengue fever, yellow fever and Zika. The present spread of resistance against pyrethroids, the primary insecticides used for mosquito control, in global populations of this species is of great concern. The voltage-gated sodium channel (VGSC) in the nervous system is the known target site of pyrethroids in insects. Past studies have revealed several amino-acid substitutions in this channel that confer pyrethroid resistance, which are known as knockdown resistance (kdr) mutations.

resultsThis study investigated a laboratory colony of Ae. aegypti, MCNaeg, established from larvae collected in Rio de Janeiro, Brazil in 2016. The MCNaeg colony showed strong resistance against pyrethroids without laboratory selection. Of the two VGSC gene haplotypes present within this colony, one harbored three known kdr mutations, V410L, V1016I, and F1534C, and the other harbored only the known F1534C mutation. In latter haplotype, we also found novel amino-acid substations including V253F. Previous molecular modeling and electrophysiological studies suggest that this residue serves a pyrethroid-sensing site in the second receptor, PyR2. Our genetical analysis showed that the haplotype harboring V253F and F1534C is associated with equal or slightly stronger resistance than the other triple kdr haplotype to both Type I and Type II pyrethroids.

conclusionThe novel substitution V253F is potentially involved in pyrethroid resistance in Ae. aegypti. Further studies are needed to elucidate the role of this substitution in the pyrethroid susceptibility of VGSC. © 2021 The Authors. Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.

Indexed as

AedesInsecticidesPyrethrinsVoltage-Gated Sodium ChannelsZika VirusZika Virus InfectionAnimalsBrazilInsecticide ResistanceMutationInsecticidesPyrethrinsVoltage-Gated Sodium ChannelsAedes aegyptiknockdown resistancepyrethroidssodium channel

Identifiers

PMID33559956
PMCPMC8247860
OpenAlexW3126424258

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.