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Fat Body Organ Culture System in Aedes Aegypti, a Vector of Zika Virus
Published on: August 19, 2017
Parallel evolution of vgsc mutations at domains IS6, IIS6 and IIIS6 in pyrethroid resistant Aedes aegypti from Mexico
Karla Saavedra-Rodriguez1, Farah Vera Maloof1, Corey L Campbell1
1Arthropod-borne and Infectious Disease Laboratory, Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, Colorado, United States of America.
Abstract:
Aedes aegypti is the primary urban mosquito vector of viruses causing dengue, Zika and chikungunya fevers -for which vaccines and effective pharmaceuticals are still lacking. Current strategies to suppress arbovirus outbreaks include removal of larval-breeding sites and insecticide treatment of larval and adult populations. Insecticidal control of Ae. aegypti is challenging, due to a recent rapid global increase in knockdown-resistance (kdr) to pyrethroid insecticides. Widespread, heavy use of pyrethroid space-sprays has created an immense selection pressure for kdr, which is primarily under the control of the voltage-gated sodium channel gene (vgsc). To date, eleven replacements in vgsc have been discovered, published and shown to be associated with pyrethroid resistance to varying degrees. In Mexico, F1,534C and V1,016I have co-evolved in the last 16 years across Ae. aegypti populations. Recently, a novel replacement V410L was identified in Brazil and its effect on vgsc was confirmed by electrophysiology. Herein, we screened V410L in 25 Ae. aegypti historical collections from Mexico, the first heterozygote appeared in 2002 and frequencies have increased in the last 16 years alongside V1,016I and F1,534C. Knowledge of the specific vgsc replacements and their interaction to confer resistance is essential to predict and to develop strategies for resistance management.
Insights
Pyrethroid insecticide resistance in Aedes aegypti mosquitoes is increasing due to genetic mutations. A new mutation, V410L, has emerged in Mexico, alongside existing resistance genes, complicating control efforts.
Area of Science:
- Medical Entomology
- Molecular Entomology
- Insecticide Resistance
Background:
- Aedes aegypti mosquitoes transmit dengue, Zika, and chikungunya viruses, with limited treatment options.
- Insecticidal control is challenged by widespread pyrethroid resistance in mosquito populations.
- Knockdown resistance (kdr) mutations in the voltage-gated sodium channel gene (vgsc) are a primary driver of pyrethroid resistance.
Purpose of the Study:
- To investigate the prevalence and evolution of the V410L vgsc mutation in Mexican Aedes aegypti populations.
- To understand the interaction of V410L with other known kdr mutations (F1,534C, V1,016I) in conferring insecticide resistance.
- To inform resistance management strategies for Aedes aegypti control.
Main Methods:
- Screening of 25 historical Aedes aegypti collections from Mexico for the V410L mutation.
- Analysis of mutation frequencies over the last 16 years.
- Comparison of V410L prevalence with co-occurring mutations F1,534C and V1,016I.
Main Results:
- The V410L mutation was detected in Mexican Aedes aegypti populations, with the first heterozygote identified in 2002.
- V410L frequencies have increased over the past 16 years.
- The emergence and rise of V410L occurred alongside increasing frequencies of V1,016I and F1,534C mutations.
Conclusions:
- The V410L mutation is spreading in Mexican Aedes aegypti populations and co-evolving with other kdr mutations.
- Understanding these specific vgsc mutations and their interactions is crucial for effective insecticide resistance management.
- This knowledge will aid in predicting and developing sustainable strategies to control arbovirus vectors.
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