目的 了解贵州省安顺市白纹伊蚊对拟除虫菊酯类杀虫剂的抗药性及代谢酶活性水平，以及其击倒抗性基因（kdr）的基因型及分布特点，为白纹伊蚊化学防控提供理论依据。方法 于2023年7月—2024年12月在安顺市不同方位的居民区小型积水容器中采集白纹伊蚊幼蚊，带回实验室饲养至F1~F2代。采用幼虫浸渍法分别测定敏感品系及野外品系Ⅲ龄末Ⅳ龄初幼蚊对溴氰菊酯、高效氯氰菊酯及氯菊酯的抗药性，采用接触筒法测定野外品系羽化后3~5 d未吸血雌蚊对3种拟除虫菊酯类杀虫剂的抗药性。酶标仪法检测未经生物测定的幼蚊非特异性酯酶（NSE）、多功能氧化酶（MFO）和谷胱甘肽-S-转移酶（GST）的活性。提取完成生物测定后单只成蚊基因组DNA，PCR扩增电压门控钠离子通道（vgsc）基因部分片段，测序后与NCBI参考序列进行比对，分析V1016、I1532、F1534、D1763位点突变及频率分布情况。采用SPSS 31.0专业版软件分析幼蚊对每种杀虫剂抗性级别，并对酶活力分布进行Shapiro-Wilk检验及Wilcoxon秩和检验，使用分类回归树算法（CART）预测代谢抗性机制与击倒抗性机制对白纹伊蚊抗药性产生的相对重要性。结果 白纹伊蚊幼蚊对溴氰菊酯、高效氯氰菊酯及氯菊酯的抗性倍数分别为38.47、18.21、209.17倍，均呈中高抗性水平；成蚊死亡率分别为2.04%（2/98）、2.06%（2/97）和7.00%（7/100），均为抗性种群。白纹伊蚊野外品系NSE、MFO、GST活力分别为356.17（321.65~497.79）nmol α-萘酚/（min·mg pr）、12.88（11.17~18.01）nmol cyt c/mg pr、128.70（116.63~153.03）nmol/（min·mg pr），均呈正偏态分布，是敏感品系的1.26、0.45和1.65倍，差异有统计学意义（Z = -4.030、-8.191、-7.371，均P < 0.01）。安顺市白纹伊蚊kdr基因除1763位点未发生突变外，在V1016、I1532、F1534位点均检测到突变，其中1016及1532位点基因型均以野生型纯合子为主（ 65.97%、98.61%）、野生/突变型杂合子次之（30.9%、1.39%）、突变型纯合子所占比例最低（3.13%、0），而1534位点有3种等位基因，即野生型（TTC/F）和突变型（TCC/S和TGC/C），其中突变型（TCC/S）的基因频率高于野生型（TTC/F），该位点突变型纯合子（S/S）的基因型频率最高，为61.11%，野生/突变型杂合子（F/S）次之，为28.47%，野生型纯合子（F/F）基因型频率为7.64%，突变型纯合子（C/C）的基因型频率最低，为2.78%。3个位点联合突变共检测到10种基因型组合，其中T1型（V/V + I/I + S/S）组合占比最高（60.76%，175/288）、T2型（V/G + I/I + F/S）组合次之（25.69%，74/288）。CART分析结果显示，安顺市白纹伊蚊对拟除虫菊酯类杀虫剂抗药性产生的相对重要性顺序依次为：1534位点突变（100%）、MFO活性（96.7%）、GST活性（66.6%），NSE活性（21.4%）、1016位点突变（16.4%）、1532位点突变（1.2%）。结论 安顺市白纹伊蚊对拟除虫菊酯类杀虫剂已产生不同程度的抗药性，体内NSE、MFO及GST活性尚未显示出代谢型抗药性特征，kdr基因以F1534位点突变为主，抗药性产生的机制是代谢解毒酶活性变化和基因突变协同作用。

Objective To investigate the resistance to pyrethroid insecticides and metabolic enzyme levels in Aedes albopictus from Anshun City, Guizhou Province, and to analyze the genotypes and distribution characteristics of the knockdown resistance (kdr) gene, so as to provide a theoretical basis for the chemical control of Ae. albopictus. Methods The larvae of Ae. albopictus were captured from small water containers in residential areas at different locations of Anshun City from July 2023 to December 2024, and then reared in laboratory to F1 to F2 generations. The resistance to deltamethrin, beta-cypermethrin and permethrin was tested in late 3rd-instar and early 4th-instar mosquito larvae of the susceptible strain and field strain with the larval dipping method, and the resistance to the three pyrethroid insecticides was determined in non-blood-fed female adults of the field strain 3 to 5 days following emergence with the tube-test method. The activity of non-specific esterase (NSE), mixed function oxidase (MFO), and glutathione-S-transferase (GST) was measured with a microplate reader in larval mosquitoes without bioassay. Genomic DNA was extracted from individual adult mosquito after bioassay, and partial fragments of the voltage-gated sodium channel (vgsc) gene were amplified using PCR assay. Following sequencing, the sequences were aligned with reference sequences from NCBI to analyze the mutations and frequency distributions of loci V1016, I1532, F1534 and D1763, respectively. The degree of resistance to pyrethroid insecticides in larval mosquitoes was graded using the software SPSS 31.0 professional, and Shapiro-Wilk test and Wilcoxon rank-sum test were performed to determine the distribution of enzyme activity. In addition, the relative importance of metabolic mechanisms and kdr mechanisms in insecticide resistance in Ae. albopictus were predicted by the classification and regression trees (CART) algorithm. Results Larvae of Ae. albopictus exhibited resistance ratios of 38.47, 18.21 and 209.17-fold to deltamethrin, beta-cypermethrin and permethrin, respectively, all appearing a moderate to high resistance level. The mortality rates of adult mosquitoes were 2.04% (2/98), 2.06% (2/97)and 7.00% (7/100), respectively, indicating resistance to all three pyrethroid insecticides. The activities of NSE, MFO, and GST were 356.17 (321.65 to 497.79) nmol α-naphthol/(min·mg pr), 12.88 (11.17 to 18.01) nmol cyt c/mg pr, and 128.70 (116.63 to 153.03) nmol/(min·mg pr) in the field population of Ae. albopictus, respectively, all showing a positively skewed distribution, which were 1.26, 0.45, and 1.65 times higher than those in susceptible strains (Z = ‒4.030, ‒8.191 and ‒7.371, all P values < 0.01). kdr gene mutations were not detected at the locus 1763 in Ae. albopictus from Anshun City, and were detected at loci V1016, I1532, and F1534. At loci 1016 and 1532, wild-type homozygotes were predominant genotypes (65.97%, 98.61%), followed by wild-type/mutant heterozygotes (30.9%, 1.39%), with the lowest proportion seen for the mutant homozygotes (3.13%, 0). There were three alleles at locus 1534, including wild-type (TTC/F), mutant (TCC/S) and mutant (TGC/C), and the mutant-type (TCC/S) had a higher gene frequency than the wild-type (TTC/F). At locus 1534, the mutant homozygote (S/S) had the highest genotype frequency (61.11%), followed by the wild/mutant-type heterozygote (F/S) (28.47%) and wild-type homozygote (F/F) (7.64%), and the mutant homozygote (C/C) had the lowest genotype frequency (2.78%). A total of 10 genotype combinations were detected in the three-locus mutation test, and the T1 genotype (V/V + I/I + S/S) accounted for the highest proportion (60.76%, 175/288), followed by the T2 genotype (V/G + I/I + F/S) (25.69%, 74/288). Results from CART analysis showed that the factors contributing to pyrethroid resistance in Ae. albopictus in Anshun City included mutation at locus 1534 (100%), MFO activity (96.7%), GST activity (66.6%), NSE activity (21.4%), mutation at locus 1016 (16.4%), and mutation at locus 1532 (1.2%). Conclusion Ae. albopictus has developed resistance to pyrethroid insecticides at varying degrees in Anshun City. The NSE, MFO or GST activities have not yet presented typical characteristics of metabolic resistance, and kdr gene mutation is dominated at locus F1534. Emergency of resistance to pyrethroid insecticides in Ae. albopictus results from the synergistic effect of changes in metabolic detoxification enzyme activities and gene mutations.