scholarly journals IDENTIFICATION OF THE kdr MUTATIONS IN VGSC GENE OF THE DENGUE MOSQUITOES AEDES ALBOPICTUS COLLECTED FROM HANOI AND HAIPHONG

2018 ◽  
Vol 16 (2) ◽  
pp. 273-278
Author(s):  
Nguyen Thi Kim Lien ◽  
Nguyen Thu Hien ◽  
Nguyen Huy Hoang ◽  
Nguyen Thi Hong Ngoc ◽  
Nguyen Thi Huong Binh
Keyword(s):  
Sodium Channel ◽  
Aedes Albopictus ◽  
Novel Mutation ◽  
Resistance Mechanism ◽  
Resistance Mechanisms ◽  
Resistance Mutations ◽  
Well Control ◽  
Voltage Gated ◽  
Activity Of Enzymes ◽  
Dengue Epidemic

Vietnam is one of the countries that is affected by dengue fever in Southeast Asia. The dengue epidemic is becoming increasingly more complex so it is necessary to have a well control to vectors in order to limit the spread of the disease. The Aedes albopictus mosquito is determined as one of the two major vectors that transmitted the dengue. Recent research shows that A. albopictus is present in some parts of Hanoi and Haiphong. In order to control the vector as well as the disease, it is necessary to understand the level of resistance and the resistance mechanism of the vector. Two important resistance mechanisms of insect were known as the mutations in the target protein of the insecticides and enhancing the activity of enzymes that participate in the resolution of the insecticides. In this study, the mosquito samples were collected from Hanoi and Haiphong to identify the level of resistance and detect the knock down resistance mutations in voltage gated sodium channel (VGSC) in membrane of nervecell of mosquito. The results of insecticide susceptibility test showed that A. albopictus in Hanoi and Haiphong were still sensitive to organophosphate but resistant to DDT, carbamate and pyrethroid. Ser989Pro, Ile1011Met, Val1016Gly and Phe1534Cys mutations were not deteced in A. albopictus in Hanoi and Haiphong. However, we detected a novel mutation Tyr986His in VGSC protein.

scholarly journals Sodium channel toxin-resistance mutations do not govern batrachotoxin (BTX) autoresistance in poison birds and frogs

2020 ◽  
Author(s):  
Fayal Abderemane-Ali ◽  
Nathan D. Rossen ◽  
Megan E. Kobiela ◽  
Robert A. Craig ◽  
Catherine E. Garrison ◽  
...  
Keyword(s):  
Sodium Channel ◽  
Small Molecule ◽  
Resistance Mechanism ◽  
Resistance Mutations ◽  
Poison Frog ◽  
Poison Frogs ◽  
Toxin Resistance ◽  
Voltage Gated ◽  
Channel Function ◽  
Toxin Sequestration

AbstractPoisonous organisms carry small molecule toxins that alter voltage-gated sodium channel (Na✓) function. Among these, batrachotoxin (BTX) from Pitohui toxic birds and Phyllobates poison frogs, stands out because of its lethality and unusual effects on Nav function. How these toxin-bearing organisms avoid autointoxication remains poorly understood. In poison frogs, a Nav DIVS6 pore-forming helix N→T mutation has been proposed as the BTX resistance mechanism. Here, we show that this variant is absent from Pitohui and poison frog Navs, incurs a strong cost that compromises channel function, and fails to produce BTX-resistant channels when tested in the context of poison frog Navs. We further show that captive-raised poison frogs are BTX resistant, even though they bear BTX-sensitive Navs. Hence, our data refute the hypothesis that BTX autoresistance is rooted in Nav mutations and instead suggest that more generalizable mechanisms such as toxin sequestration act to protect BTX-bearing species from autointoxication.

scholarly journals Polymorphisms in voltage-gated sodium channel gene and susceptibility of Aedes albopictus to insecticides in three districts of northern West Bengal, India

2018 ◽  
Vol 12 (1) ◽  
pp. e0006192 ◽  
Author(s):  
Moytrey Chatterjee ◽  
Sudeep Ballav ◽  
Ardhendu K. Maji ◽  
Nandita Basu ◽  
Biplab Chandra Sarkar ◽  
...  
Keyword(s):  
Sodium Channel ◽  
Aedes Albopictus ◽  
West Bengal ◽  
Voltage Gated Sodium Channel ◽  
Voltage Gated ◽  
Channel Gene ◽  
Sodium Channel Gene

scholarly journals Multi-country Survey Revealed Prevalent and Novel F1534S Mutation in Voltage-Gated Sodium Channel (VGSC) Gene in Aedes albopictus

2016 ◽  
Vol 10 (5) ◽  
pp. e0004696 ◽  
Author(s):  
Jiabao Xu ◽  
Mariangela Bonizzoni ◽  
Daibin Zhong ◽  
Guofa Zhou ◽  
Songwu Cai ◽  
...  
Keyword(s):  
Sodium Channel ◽  
Aedes Albopictus ◽  
Voltage Gated Sodium Channel ◽  
Voltage Gated

scholarly journals Evidence that toxin resistance in poison birds and frogs is not rooted in sodium channel mutations and may rely on “toxin sponge” proteins

2021 ◽  
Vol 153 (9) ◽  
Author(s):  
Fayal Abderemane-Ali ◽  
Nathan D. Rossen ◽  
Megan E. Kobiela ◽  
Robert A. Craig ◽  
Catherine E. Garrison ◽  
...  
Keyword(s):  
Ion Channel ◽  
Sodium Channel ◽  
Small Molecule ◽  
Resistance Mechanism ◽  
Poison Frog ◽  
Poison Frogs ◽  
Toxin Resistance ◽  
Voltage Gated ◽  
Primary Driver ◽  
Toxin Sequestration

Many poisonous organisms carry small-molecule toxins that alter voltage-gated sodium channel (NaV) function. Among these, batrachotoxin (BTX) from Pitohui poison birds and Phyllobates poison frogs stands out because of its lethality and unusual effects on NaV function. How these toxin-bearing organisms avoid autointoxication remains poorly understood. In poison frogs, a NaV DIVS6 pore-forming helix N-to-T mutation has been proposed as the BTX resistance mechanism. Here, we show that this variant is absent from Pitohui and poison frog NaVs, incurs a strong cost compromising channel function, and fails to produce BTX-resistant channels in poison frog NaVs. We also show that captivity-raised poison frogs are resistant to two NaV-directed toxins, BTX and saxitoxin (STX), even though they bear NaVs sensitive to both. Moreover, we demonstrate that the amphibian STX “toxin sponge” protein saxiphilin is able to protect and rescue NaVs from block by STX. Taken together, our data contradict the hypothesis that BTX autoresistance is rooted in the DIVS6 N→T mutation, challenge the idea that ion channel mutations are a primary driver of toxin resistance, and suggest the possibility that toxin sequestration mechanisms may be key for protecting poisonous species from the action of small-molecule toxins.

scholarly journals KÊNH DẪN TRUYỀN NA+ CỔNG ĐIỆN ÁP (NaV) VÀ TÍNH KHÁNG THUỐC DIỆT CÔN TRÙNG Ở MUỖI TRUYỀN BỆNH SỐT XUẤT HUYẾT

2017 ◽  
Vol 15 (3) ◽  
pp. 393-401
Author(s):  
Nguyễn Thị Kim Liên ◽  
Nguyễn Thị Hương Bình
Keyword(s):  
Aedes Aegypti ◽  
Sodium Channel ◽  
Aedes Albopictus ◽  
Voltage Gated Sodium Channel ◽  
Voltage Gated

Bệnh sốt xuất huyết là bệnh truyền nhiễm cấp tính, có thể gây thành dịch lớn và có tỷ lệ tử vong cao. Bệnh lưu hành trên hơn 100 quốc gia trên thế giới ở hầu hết các châu lục. Sốt xuất huyết được lây truyền qua vector trung gian là muỗi Aedes (Aedes aegypti và Aedes albopictus). Việc kiểm soát vector truyền bệnh đóng vai trò quan trọng trong việc ngăn ngừa sự bùng phát của dịch. Trong các biện pháp kiểm soát vector truyền bệnh, việc sử dụng thuốc diệt côn trùng đã mang lại những hiệu quả đáng kể và thuốc diệt côn trùng được sử dụng rộng rãi hiện nay thuộc nhóm pyrethroid. Các hóa chất thuộc nhóm pyrethroid chủ yếu tác động lên côn trùng thông qua các thụ thể trên kênh dẫn truyền Na+ của các neuron thần kinh ở côn trùng. Pyrethroid cản trở sự ngừng hoạt động của kênh dẫn truyền, kết quả là kênh K+ mở trong thời gian dài làm gián đoạn tín hiệu điện trong hệ thống thần kinh, làm mất khả năng bay của côn trùng. Tuy nhiên, khả năng kháng thuốc ở côn trùng trong đó có muỗi đang khiến cho hiệu quả của thuốc diệt côn trùng bị giảm đi. Khả năng kháng thuốc được xác định là do các đột biến trên gen mã hóa cho kênh dẫn truyền Na+ (voltage-gated sodium channel – VGSC). Cho đến nay, rất nhiều đột biến đã được xác định có liên quan đến tính kháng ở các quần thể muỗi Aedes. Thêm vào đó, tần xuất của các đột biến trên gen VGSC ở các quần thể muỗi khác nhau có sự khác biệt rất lớn. Vì vậy, nghiên cứu tính kháng thuốc diệt ở muỗi Aedes sẽ giúp cho việc kiểm soát tốt đối với vector truyền bệnh sốt xuất huyết.

scholarly journals Molecular Insight into the Knockdown Resistance (kdr) in the Voltage Gated Sodium Channel (vgsc) Gene of the Main Dengue Vector, Aedes aegypti (Diptera: Culicidae) and the Discovery of Novel Regional Specific Point Mutation A1007G in Malaysia.

2021 ◽  
Author(s):  
Mas Azlin M. Akhir ◽  
Mustafa F. F. Wajidi ◽  
Sébastien Lavoué ◽  
Ghows Azzam ◽  
Izhan Shahrin Jaafar ◽  
...  
Keyword(s):  
Insecticide Resistance ◽  
Sodium Channel ◽  
Vector Control ◽  
Resistance Mechanism ◽  
Point Mutations ◽  
Voltage Gated Sodium Channel ◽  
Pyrethroid Insecticides ◽  
Voltage Gated ◽  
Control Programmes ◽  
Pirimiphos Methyl

Abstract Background: Characterization of the insecticide resistance mechanism imparts the society with the information on the evolutionary process involved in the adaptation of Aedes aegypti mosquito to environmental changes. Investigating the phenotypic status of the target mosquitoes, their resistance level as well as elucidating the genotypic profile provides information about the involvement of insecticide resistance mechanism, in terms of portraying the evolution of resistance in the field, to eventually managing vector control programmes. In this current study, we investigated the quantification responses for the phenotypic and genotypic resistance of Ae. aegypti population from different states in Malaysia. Methods: We tested insecticide susceptibility status of adult Ae. aegypti from populations of States of Penang, Selangor and Kelantan (Peninsular Malaysia) against 0.25% permethrin and 0.25% pirimiphos-methyl through WHO bioassay kit. Permethrin-resistant and permethrin susceptible samples were then genotyped for domains II and III in the voltage gated sodium channel (vgsc) gene using allele specific PCR (AS-PCR) for the presence of diagnostic single nucleotide mutations. AS-PCR results were then validated in sequencing these two domains to identify any possible additional point mutations. Results: Adult WHO bioassay revealed that populations of Ae. aegypti from these three states were highly resistant towards 0.25% permethrin and 0.25% pirimiphos-methyl. Genotyping results showed that three knockdown (kdr) mutations (i.e. S989P, V1016G and F1534C) were associated with pyrethroid resistance in these populations. We also report for the first time the presence of the A1007G mutation in Malaysian populations of Ae. aegypti.Conclusions: This study brings an insight on the occurrence and association of point mutations with insecticide resistance in Malaysian populations of Ae. aegypti. The results reveal the widespread of several kdr mutations in the field with the consequence to compromise the use of pyrethroid insecticides in vector control programmes. Knowledge on the distribution of target site resistance throughout Malaysia is vital to ensure the success of the insecticide-based vector control programme.

scholarly journals Frequency of sodium channel genotypes and association with pyrethrum knockdown time in populations of Californian Aedes aegypti

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Lindsey K. Mack ◽  
Erin Taylor Kelly ◽  
Yoosook Lee ◽  
Katherine K. Brisco ◽  
Kaiyuan Victoria Shen ◽  
...  
Keyword(s):  
Los Angeles ◽  
Aedes Aegypti ◽  
Sodium Channel ◽  
Central Valley ◽  
Resistance Mechanisms ◽  
Significant Heterogeneity ◽  
Residential Areas ◽  
Breeding Sites ◽  
Voltage Gated ◽  
The Individual

AbstractBackgroundSince their detection in 2013,Aedes aegyptihas become a widespread urban pest in California. The availability of cryptic larval breeding sites in residential areas and resistance to insecticides pose significant challenges to control efforts. Resistance to pyrethroids is largely attributed to mutations in the voltage gated sodium channels (VGSC), the pyrethroid site of action. However, past studies have indicated that VGSC mutations may not be entirely predictive of the observed resistance phenotype.MethodsTo investigate the frequencies of VGSC mutations and the relationship with pyrethroid insecticide resistance in California, we sampledAe. aegyptifrom four locations in the Central Valley, and the Greater Los Angeles area. Mosquitoes from each location were subjected to an individual pyrethrum bottle bioassay to determine knockdown times. A subset of assayed mosquitoes from each location was then analyzed to determine the composition of 5 single nucleotide polymorphism (SNP) loci within the VGSC gene.ResultsThe distribution of knockdown times for each of the five Californian populations sampled was non-parametric with potentially bimodal distributions. One group succumbs to insecticidal effects around 35–45 min and the second group lasts up to and beyond the termination of the assay (120+ min). We detected 5 polymorphic VGSC SNPs within the sampled California populations. One is potentially new and alternatively spliced (I915K), and four are documented and associated with resistance: F1534C, V1016I, V410L and S723T. The Central Valley populations (Clovis, Dinuba, Sanger and Kingsburg) are fairly homogenous with only 5% of the mosquitoes showing heterozygosity at any given position. In the Greater LA mosquitoes, 55% had at least one susceptible allele at any of the five SNP loci. The known resistance allele F1534C was detected in almost all sampled mosquitoes (99.4%). We also observe significant heterogeneity in the knockdown phenotypes of individuals with the identical VGSC haplotypes suggesting the presence of additional undefined resistance mechanisms.ConclusionsResistance associated VGSC SNPs are prevalent, particularly in the Central Valley. Interestingly, among mosquitoes carrying all 4 resistance associated SNPs, we observe significant heterogeneity in bottle bioassay profiles suggesting that other mechanisms are important to the individual resistance ofAe. aegyptiin California. Keywords:Aedes aegypti, Resistance, Pyrethroid, IPLEX genotyping, Voltage gated sodium channel, California.

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