诱导结核分枝杆菌耐katG基因突变过程的分析  

Preliminary study on inducing gene mutation process of mycobacterium tuberculosis

作　　者：杨楠[1] 张广宇[1] 刘璠 李洪敏[1] 刘银萍[1] 杨栗坤[1] 张霞[1] 

机构地区：[1]解放军第309医院结核病研究所,北京100091 [2]秦皇岛市海港区港口医院老干部科,066000

出　　处：《国际呼吸杂志》2012年第14期1055-1057,共3页International Journal of Respiration

摘　　要：目的在体外建立诱导结核分枝杆菌耐异烟肼药物产生的全过程，分析结核分枝杆菌产生耐药的机理。方法对结核分枝杆菌强毒株（H37RV）进行诱导试验，与30株临床耐异烟肼药物分离株共同做聚合酶链反应一单链构象多态性（PCR—SSCP）和序列分析。结果在第7代H37RV的PCR—SSCP电泳出现异常，经测序证实发生katG基因突变，与部分临床突变株的类型基本相同。结论用药物间断性地不断刺激结核分枝杆菌，是产生结核分枝杆菌耐异烟肼药物的重要原因之一。Objective To preliminarily analyze the mechanism of drug resistance tuberculosis by observing the entire process of isoniazid-resistant tuberculosis in vitro experiments. Methods The tuberculosis virulent strain （H37RV） induced in the different levels of drug and 30 isolated strains of clinical drug resistance were detected by polymerase chain reaction-single strand conformation pofymorphism （FCR-SSCP） and sequence analysis. Results PCR-SSCP electrophoresis was abnormal in 7th generation of H37RV. Confirmed by sequencing, katG gene occurred mutation, same as clinical mutant type. Conclusions Stimulating constantly tubercle bacillus with drug is an important reason that causes isoniazidresistance.

关 键 词：结核分枝杆菌 诱导 聚合酶链反应一单链构象多态性 测序 

分 类 号：R52[医药卫生—内科学]