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Detection of a new pyrethroid resistance mutation (V410L) in the sodium channel of Aedes aegypti: a potential challenge for mosquito control.
Haddi K
,
Tomé HVV
,
Du Y
,
Valbon WR
,
Nomura Y
,
Martins GF
,
Dong K
,
Oliveira EE
.
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The yellow fever mosquito, Aedes aegypti, particularly in Neotropical regions, is the principal vector of dengue, yellow fever, Zika and Chikungunya viruses. Pyrethroids remain one of the most used insecticides to control Aedes mosquitoes, despite the development of pyrethroid resistance in many mosquito populations worldwide. Here, we report a Brazilian strain of A. aegypti with high levels (approximately 100-60,000 fold) of resistance to both type I and type II pyrethroids. We detected two mutations (V410L and F1534C) in the sodium channel from this resistant strain. This study is the first report of the V410L mutation in mosquitoes. Alone or in combination with the F1534C mutation, the V410L mutation drastically reduced the sensitivity of mosquito sodium channels expressed in Xenopus oocytes to both type I and type II pyrethroids. The V410L mutation presents a serious challenge for the control of A. aegypti and will compromise the use of pyrethroids for the control of A. aegypti in Brazil; therefore, early monitoring of the frequency of the V410L mutation will be a key resistance management strategy to preserve the effectiveness of pyrethroid insecticides.
Figure 1. Toxicity (a,b) and comparative effects of synergists (c,d) on mortality caused by permethrin and deltamethrin to larvae (L4) of two Brazilian strains of Aedes aegypti. (a,b) The lines denote the lethal concentration (LC) values estimated based on concentration-mortality bioassays using probit analyses. Symbols show the averaged mortality for each insecticide concentration applied to each population of A. aegypti. The vertical bars represent the standard error of the average (SE). (c,d) The effects of the synergists piperonyl butoxide (PBO), diethyl maleate (DEM) and triphenyl phosphate (TPP) on the mortality of the resistant population caused by pyrethroids at the LC50 obtained for the resistant strain. Asterisks indicate significant differences in relation to the unsynergized insecticide (one-way ANOVA with Scheffe’s post hoc analysis, P < 0.05).
Figure 2. Toxicity (a,b) and comparative effects of synergists (c,d) on mortality caused by permethrin and deltamethrin to adults of two Brazilian strains of Aedes aegypti. (a,b) The lines denote the lethal concentration (LC) values estimated based on concentration-mortality bioassays using probit analyses. Symbols show the averaged mortality for each insecticide concentration applied to each population of A. aegypti. The vertical bars represent the standard error of the average (SE). (c,d) The effects of the synergists piperonyl butoxide (PBO), diethyl maleate (DEM) and triphenyl phosphate (TPP) on the mortality of the resistant population caused by pyrethroids at the LC50 obtained for the resistant strain. Asterisks indicate significant differences in relation to the unsynergized insecticide (one-way ANOVA with Scheffe’s post hoc analysis, P < 0.05).
Figure 3. Pyrethroid resistance-associated amino acid substitutions in A. aegypti sodium channels. (a) Schematic representation of the mosquito sodium channel protein (AaNav1-1) indicating two knockdown resistance mutations in IS6 and IVS6. Sodium channels are large transmembrane proteins with four homologous repeats (I–IV), each having six transmembrane segments (S1–S6). Residue positions correspond to the cockroach BgNav protein (GenBank number: U73583). Dose-response curves of permethrin (b) and deltamethrin (c) on BgNav1-1a, V410L, F1534C and V410L + F1534C cockroach sodium channels. The method for determining the percentage of modified channels is described in the Materials & Methods section.
Bellinato,
Resistance Status to the Insecticides Temephos, Deltamethrin, and Diflubenzuron in Brazilian Aedes aegypti Populations.
2016, Pubmed
Bellinato,
Resistance Status to the Insecticides Temephos, Deltamethrin, and Diflubenzuron in Brazilian Aedes aegypti Populations.
2016,
Pubmed
Brito,
Assessing the effects of Aedes aegypti kdr mutations on pyrethroid resistance and its fitness cost.
2013,
Pubmed
Chapadense,
Phenotypic and genotypic profile of pyrethroid resistance in populations of the mosquito Aedes aegypti from Goiânia, Central West Brazil.
2015,
Pubmed
Chediak,
Spatial and temporal country-wide survey of temephos resistance in Brazilian populations of Aedes aegypti.
2016,
Pubmed
Davies,
A comparative study of voltage-gated sodium channels in the Insecta: implications for pyrethroid resistance in Anopheline and other Neopteran species.
2007,
Pubmed
Devine,
Using adult mosquitoes to transfer insecticides to Aedes aegypti larval habitats.
2009,
Pubmed
Dong,
Molecular biology of insect sodium channels and pyrethroid resistance.
2014,
Pubmed
Du,
Rotational Symmetry of Two Pyrethroid Receptor Sites in the Mosquito Sodium Channel.
2015,
Pubmed
Du,
A negative charge in transmembrane segment 1 of domain II of the cockroach sodium channel is critical for channel gating and action of pyrethroid insecticides.
2010,
Pubmed
Du,
Molecular evidence for dual pyrethroid-receptor sites on a mosquito sodium channel.
2013,
Pubmed
,
Xenbase
Feng,
Cloning and functional analysis of TipE, a novel membrane protein that enhances Drosophila para sodium channel function.
1995,
Pubmed
,
Xenbase
Hemingway,
An overview of insecticide resistance.
2002,
Pubmed
Hemingway,
The molecular basis of insecticide resistance in mosquitoes.
2004,
Pubmed
Hirata,
A single crossing-over event in voltage-sensitive Na+ channel genes may cause critical failure of dengue mosquito control by insecticides.
2014,
Pubmed
,
Xenbase
Hu,
A sodium channel mutation identified in Aedes aegypti selectively reduces cockroach sodium channel sensitivity to type I, but not type II pyrethroids.
2011,
Pubmed
,
Xenbase
Jones,
Footprints of positive selection associated with a mutation (N1575Y) in the voltage-gated sodium channel of Anopheles gambiae.
2012,
Pubmed
Linss,
Distribution and dissemination of the Val1016Ile and Phe1534Cys Kdr mutations in Aedes aegypti Brazilian natural populations.
2014,
Pubmed
Liu,
Multiple Cytochrome P450 genes: their constitutive overexpression and permethrin induction in insecticide resistant mosquitoes, Culex quinquefasciatus.
2011,
Pubmed
Liu,
Insecticide resistance in mosquitoes: impact, mechanisms, and research directions.
2015,
Pubmed
Marriel,
Deltamethrin-mediated survival, behavior, and oenocyte morphology of insecticide-susceptible and resistant yellow fever mosquitos (Aedes aegypti).
2016,
Pubmed
O'Reilly,
Modelling insecticide-binding sites in the voltage-gated sodium channel.
2006,
Pubmed
Oliveira,
A residue in the transmembrane segment 6 of domain I in insect and mammalian sodium channels regulate differential sensitivities to pyrethroid insecticides.
2013,
Pubmed
,
Xenbase
Ranson,
Insecticide Resistance in African Anopheles Mosquitoes: A Worsening Situation that Needs Urgent Action to Maintain Malaria Control.
2016,
Pubmed
Reiter,
Control of Urban Zika Vectors: Should We Return to the Successful PAHO/WHO Strategy?
2016,
Pubmed
Rinkevich,
Diversity and Convergence of Sodium Channel Mutations Involved in Resistance to Pyrethroids.
2013,
Pubmed
Scott,
Cytochromes P450 and insecticide resistance.
1999,
Pubmed
Silver,
Voltage-Gated Sodium Channels as Insecticide Targets.
2014,
Pubmed
Smith,
Pyrethroid resistance in Aedes aegypti and Aedes albopictus: Important mosquito vectors of human diseases.
2016,
Pubmed
Soderlund,
Molecular mechanisms of pyrethroid insecticide neurotoxicity: recent advances.
2012,
Pubmed
Soderlund,
State-Dependent Modification of Voltage-Gated Sodium Channels by Pyrethroids.
2010,
Pubmed
,
Xenbase
Tan,
Identification of amino acid residues in the insect sodium channel critical for pyrethroid binding.
2005,
Pubmed
,
Xenbase
Tatebayashi,
Differential mechanism of action of the pyrethroid tetramethrin on tetrodotoxin-sensitive and tetrodotoxin-resistant sodium channels.
1994,
Pubmed
Vais,
Activation of Drosophila sodium channels promotes modification by deltamethrin. Reductions in affinity caused by knock-down resistance mutations.
2000,
Pubmed
,
Xenbase
Warmke,
Functional expression of Drosophila para sodium channels. Modulation by the membrane protein TipE and toxin pharmacology.
1997,
Pubmed
,
Xenbase
Zhorov,
Elucidation of pyrethroid and DDT receptor sites in the voltage-gated sodium channel.
2017,
Pubmed
