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

BACKGROUND Aedes 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...

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Published inPest Management Science Vol. 77; no. 6; pp. 2887 - 2893
Main Authors Itokawa, Kentaro, Furutani, Shogo, Takaoka, Aki, Maekawa, Yoshihide, Sawabe, Kyoko, Komagata, Osamu, Tomita, Takashi, Lima Filho, José Luiz, Alves, Luiz Carlos, Kasai, Shinji
Format Journal Article
LanguageEnglish
Published Chichester, UK Wiley 01.06.2021
John Wiley & Sons, Ltd
Wiley Subscription Services, Inc
Subjects
Aedes
Aedes aegypti
amino acids
Animals
Aquatic insects
Brazil
Colonies
dengue
Dengue fever
Electric potential
Electrical transmission
electrophysiology
Epidemiology
genes
Haplotypes
Insect control
Insecticide Resistance
Insecticides
Insects
knockdown resistance
Laboratories
Larvae
Molecular modelling
mosquito control
mosquito vectors
Mosquitoes
Mutation
Nervous system
Pest control
pesticide resistance
Pyrethrins
Pyrethroids
Receptors
Sodium
sodium channel
sodium channels
Sodium channels (voltage-gated)
Substations
Substitutes
Tropical diseases
Vector-borne diseases
Voltage
Voltage-Gated Sodium Channels
Yellow fever
Zika Virus
Zika Virus Infection
Brazil
pyrethroids
Aedes aegypti
sodium channel
knockdown resistance
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Abstract BACKGROUND Aedes 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. RESULTS This 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. CONCLUSION The 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. We found a novel amino‐acid substitution V253F in the voltage‐gated sodium channel in Aedes aegypti which is potentially involved in pyrethroid resistance of this vector mosquito
AbstractList Aedes 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.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.This 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.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.The 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.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.
Aedes 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. This 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. The 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.
BACKGROUND Aedes 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. RESULTS This 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. CONCLUSION The 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. We found a novel amino‐acid substitution V253F in the voltage‐gated sodium channel in Aedes aegypti which is potentially involved in pyrethroid resistance of this vector mosquito
BACKGROUND: Aedes 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. RESULTS: This 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. CONCLUSION: The 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.
We found a novel amino‐acid substitution V253F in the voltage‐gated sodium channel in Aedes aegypti which is potentially involved in pyrethroid resistance of this vector mosquito
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.
Author José Luiz de Lima Filho
Shinji Kasai
Osamu Komagata
Takashi Tomita
Kyoko Sawabe
Shogo Furutani
Luiz Carlos Alves
Yoshihide Maekawa
Kentaro Itokawa
Aki Takaoka
AuthorAffiliation 4 Instituto Aggeu Magalhães‐FIOCRUZ/PE Recife Brazil
2 Department of Medical Entomology National Institute of Infectious Diseases Tokyo Japan
3 Laboratório de Imunopatologia Keizo Asami Universidade Federal de Pernambuco Recife Brazil
1 Pathogen Genomics Center National Institute of Infectious Diseases Tokyo Japan
AuthorAffiliation_xml – name: 1 Pathogen Genomics Center National Institute of Infectious Diseases Tokyo Japan
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2021 The Authors. Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.
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DocumentTitleAlternate A novel amino‐acid substitution, V253F, on the Aedes aegypti voltage‐gated sodium channel
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Keywords pyrethroids
Aedes aegypti
sodium channel
knockdown resistance
Language English
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2021 The Authors. Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.
This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
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Notes Shogo Furutani is co‐first author.
These authors contributed equally in this research.
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Snippet BACKGROUND Aedes aegypti is a remarkably effective mosquito vector of epidemiologically important arboviral diseases including dengue fever, yellow fever and...
Aedes aegypti is a remarkably effective mosquito vector of epidemiologically important arboviral diseases including dengue fever, yellow fever and Zika. The...
BACKGROUNDAedes aegypti is a remarkably effective mosquito vector of epidemiologically important arboviral diseases including dengue fever, yellow fever and...
BACKGROUND: Aedes aegypti is a remarkably effective mosquito vector of epidemiologically important arboviral diseases including dengue fever, yellow fever and...
We found a novel amino‐acid substitution V253F in the voltage‐gated sodium channel in Aedes aegypti which is potentially involved in pyrethroid resistance of...
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StartPage 2887
SubjectTerms Aedes
Aedes aegypti
amino acids
Animals
Aquatic insects
Brazil
Colonies
dengue
Dengue fever
Electric potential
Electrical transmission
electrophysiology
Epidemiology
genes
Haplotypes
Insect control
Insecticide Resistance
Insecticides
Insects
knockdown resistance
Laboratories
Larvae
Molecular modelling
mosquito control
mosquito vectors
Mosquitoes
Mutation
Nervous system
Pest control
pesticide resistance
Pyrethrins
Pyrethroids
Receptors
Sodium
sodium channel
sodium channels
Sodium channels (voltage-gated)
Substations
Substitutes
Tropical diseases
Vector-borne diseases
Voltage
Voltage-Gated Sodium Channels
Yellow fever
Zika Virus
Zika Virus Infection
Title A first, naturally occurring substitution at the second pyrethroid receptor of voltage‐gated sodium channel of Aedes aegypti
URI https://cir.nii.ac.jp/crid/1874242817814104320
https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fps.6324
https://www.ncbi.nlm.nih.gov/pubmed/33559956
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