Co-occurrence of point mutations in the voltage-gated sodium channel of pyrethroid-resistant Aedes aegypti populations in Myanmar.
Co-occurrence of point mutations in the voltage-gated sodium channel of pyrethroid-resistant Aedes aegypti populations in Myanmar.
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DOI：
10.1371/journal.pntd.0003032
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发表时间：
2014
影响因子：
3.8
通讯作者：
Minakawa N
中科院分区：
文献类型：
--
作者：
Kawada H;Oo SZ;Thaung S;Kawashima E;Maung YN;Thu HM;Thant KZ;Minakawa N
与拟除虫菊酯抗性相关的电压门控钠通道上的单一氨基酸替换是昆虫对拟除虫菊酯产生抗性的主要原因之一。已经在几种蚊子中观察到kdr基因；然而，缅甸埃及伊蚊种群的para基因点突变还没有完全确定。本研究的目的是确定缅甸仰光市废旧轮胎中埃及伊蚊para基因突变的类型和频率。我们用简化的基因敲除生物测定法测定了仰光市所有采集点埃及伊蚊幼虫对拟除虫菊酯的高度抗性。我们发现V1016G和S989P突变分布广泛，频率较高(分别为84.4%和78.8%)。相比之下，我们无法检测到I1011M(或I1011V)或L1014F突变。F1534C突变也广泛分布，但频率低于V1016G突变(21.2%)。V1016G/S989P纯合子突变的发生率较高(65.7%)。V1016G/F1534C纯合子突变(2.9%)和V1016G/F1534C/S989P纯合子突变(0.98%)并存。拟除虫菊酯杀虫剂于1992年首次用于疟疾控制，自那以来一直在缅甸使用。这种密集的使用可能解释了为什么对埃及伊蚊有很大的选择压力，因为这种蚊子通常是一种家养和内食蚊子，喜欢在室内繁殖。在禁止使用滴滴涕之前，广泛使用滴滴涕控制疟疾也可能解释埃及伊蚊对拟除虫菊酯产生抗药性的原因。高活性拟除虫菊酯的使用加速了媒介蚊体对拟除虫菊酯抗性的发展。敲除抗性(Kdr)等位基因在电压门控钠通道中含有单一氨基酸替换，是昆虫对拟除虫菊酯产生抗性的主要原因之一。我们调查了缅甸仰光市废旧轮胎中埃及伊蚊幼虫kdr基因的分布。发现V1016G/S989P点突变分布广泛，少量V1016G/F1534C和V1016G/F1534C/S989P点突变共存。埃及伊蚊种群。使用拟除虫菊酯和/或滴滴涕控制疟疾被认为是埃及伊蚊对拟除虫菊酯产生抗药性的主要原因之一。控制疟疾病媒的杀虫剂处理似乎在埃及伊蚊繁殖地和栖息地所在的人类居住区的内陆和外围进行了密集的处理。
Single amino acid substitutions in the voltage-gated sodium channel associated with pyrethroid resistance constitute one of the main causative factors of knockdown resistance in insects. The kdr gene has been observed in several mosquito species; however, point mutations in the para gene of Aedes aegypti populations in Myanmar have not been fully characterized. The aim of the present study was to determine the types and frequencies of mutations in the para gene of Aedes aegypti collected from used tires in Yangon City, Myanmar. We determined high pyrethroid resistance in Aedes aegypti larvae at all collection sites in Yangon City, by using a simplified knockdown bioassay. We showed that V1016G and S989P mutations were widely distributed, with high frequencies (84.4% and 78.8%, respectively). By contrast, we were unable to detect I1011M (or I1011V) or L1014F mutations. F1534C mutations were also widely distributed, but with a lower frequency than the V1016G mutation (21.2%). High percentage of co-occurrence of the homozygous V1016G/S989P mutations was detected (65.7%). Additionally, co-occurrence of homozygous V1016G/F1534C mutations (2.9%) and homozygous V1016G/F1534C/S989P mutations (0.98%) were detected in the present study. Pyrethroid insecticides were first used for malaria control in 1992, and have since been constantly used in Myanmar. This intensive use may explain the strong selection pressure toward Aedes aegypti, because this mosquito is generally a domestic and endophagic species with a preference for indoor breeding. Extensive use of DDT for malaria control before the use of this chemical was banned may also explain the development of pyrethroid resistance in Aedes aegypti. The use of pyrethroids with high killing activity has accelerated the development of pyrethroid resistance in vector mosquitoes. The knockdown resistance (kdr) allele contains a single amino acid substitution in the voltage-gated sodium channel and is one of the main causative factors of pyrethroid resistance in insects. We investigated the distribution of the kdr gene in Aedes aegypti larvae collected from used tires in Yangon City, Myanmar. We detected three patterns of co-occurrence of point mutations, namely, V1016G/S989P with wide distribution, and small number of V1016G/F1534C and V1016G/F1534C/S989P, both of which were first found in the field collected Ae. aegypti population. The use of pyrethroids and/or DDT for malaria control is thought to be one of the main causes of pyrethroid resistance in Aedes aegypti. Insecticide treatment for malaria vector control seems to have been intensively conducted in the interior and along the periphery of human habitation areas, where the breeding and resting sites of Aedes aegypti are located.
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