Wu X, Zhang J, Hu Z
Tuberculosis Research Laboratory, 309th Hospital, PLA, Beijing 100091.
Zhonghua Jie He He Hu Xi Za Zhi. 1998 Dec;21(12):727-9.
To investigate the mutations of ahpC genes in M. tuberculosis isoniazid-resistant isolates, and to study the correlation between ahpC alterations and isoniazid resistance.
Analyzing the ahpC coding sequences and ahpC promoters in 62 M. tuberculosis clinical isolates with PCR-SSCP method. M. tuberculosis strain H37RV was used as control.
The ahpC coding sequences showed normal SSCP profiles in 62 clinical isolates. AhpC promoter mutations were identified in 5 of 12 high isoniazid-resistant strains, and were not altered in 18 low isoniazid-resistant and 32 drug-sensitive isolates.
The mutation of ahpC coding gene was not correlated with isoniazid-resistant M. tuberculosis isolates. AhpC promoter mutation was a compensatory change in katG-defective and catalase-negative isolates, may be used as a indirect marker for high resistance to isoniazid.
研究结核分枝杆菌异烟肼耐药株中ahpC基因的突变情况,并探讨ahpC基因改变与异烟肼耐药性之间的相关性。
采用PCR-SSCP方法分析62株结核分枝杆菌临床分离株的ahpC编码序列和ahpC启动子。以结核分枝杆菌H37RV菌株作为对照。
62株临床分离株的ahpC编码序列显示SSCP图谱正常。在12株高异烟肼耐药菌株中有5株检测到ahpC启动子突变,18株低异烟肼耐药菌株和32株药物敏感菌株中未检测到改变。
ahpC编码基因突变与结核分枝杆菌异烟肼耐药株无关。ahpC启动子突变是katG缺陷型和过氧化氢酶阴性菌株的一种代偿性变化,可作为对异烟肼高耐药性的间接标志物。