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机构地区:[1]武汉轻工大学生物与制药工程学院,湖北武汉430023 [2]上海凯地生物科技有限公司,上海20025
出 处:《武汉轻工大学学报》2015年第3期37-40,共4页Journal of Wuhan Polytechnic University
基 金:上海市科委科技支撑项目(12441903300)
摘 要:探讨武汉地区结核分枝杆菌临床分离株异烟肼耐药相关基因突变特征。通过PCR直接序列分析法对异烟肼耐药相关基因kat G基因及mab A-inhA启动子进行序列分析。20株异烟肼敏感株未检测到突变,49株耐药株中有40株(81.6%)存在突变,其中katG的S315突变率占主导优势,突变率为73.5%(36/49),mab A-inhA启动子区核苷酸置换率为8.2%(4/49),其中一株同时检测到了katG和mabA-inhA启动子区的突变。此外,还检测到了一种国内尚未报道的katG突变类型P232S(CCG→TCG)。研究证实kat G基因和mabA-inhA启动子的突变与异烟肼耐药相关,为进一步研究结核分枝杆菌异烟肼耐药性奠定了基础。To evaluate the characteristic of genes associated with isoniazid-resistant Mycobacterium tuberculosis clinical isolates collected from Wuhan,China. Methods The genotypes of katG and mabA-inhA promoter that associated with isoniazid-resistance were analyzed with PCR direct sequencing. Results Of the 49 isoniazid-resistant clinical isolates,43 strains( 81. 6%) carried mutations in the target genes,and no mutations was found in the 20 isoniazidsensitive strains. The mutations in kat G gene at codon 315 was the most frequent mutations up to 73. 5%( 36 /49)in all. The nucleotide replacement rate of mab A-inh A promoter was 8. 2%( 4 /49). One isolate strain was detected mutations both in katG mabA-inhA promoter. Moreover,we found a new mutant type P232S( CCG→TCG). Conclusions This study confirmed that mutations in the katG and mabA-inhA promoter related with isoniazid-resistance,and provided clues to explore the mechanism of isoniazid-resistant Mycobacterium tuberculosis.
关 键 词:结核分枝杆菌 异烟肼 耐药 KATG基因 mabA-inhA启动子
分 类 号:R378[医药卫生—病原生物学]
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