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为了解结核分枝杆菌耐异烟肼（ＩＮＨ）分离株ｋａｔＧ基因和ｉｎｈＡ调节序列的突变情况，探讨其在ＩＮＨ耐药性中的可能作用。应用聚合酶链反应（ＰＣＲ）和ＰＣＲ－单链构象多态性（ＳＳＣＰ）方法对６２株结核分枝杆菌临床分离株的ｋａｔＧ基因和ｉｎｈＡ调节序列进行分析。ＰＣＲ分析结果显示：ｋａｔＧ基因和ｉｎｈＡ调节序列的敏感性为１～１０ｐｇＤＮＡ；其引物ＰＣＲ扩增都具有较高的特异性。以Ｈ３７Ｒｖ标准株为对照，１３株敏感株中，１２株ｋａｔＧ基因扩增产物ＳＳＣＰ泳动正常，１株ｋａｔＧ异常；２４株耐非ＩＮＨ抗结核药物株中，８株ｋａｔＧＳＳＣＰ异常；上述２７株的ｉｎｈＡ调节序列ＳＳＣＰ均泳动正常。２５株耐ＩＮＨ株中，３株ｋａｔＧ基因ＰＣＲ扩增阴性，２２株ｋａｔＧ扩增阳性，其中１６株ＳＳＣＰ泳动异常；４株ｉｎｈＡ调节序列ＳＳＣＰ泳动异常，其ｋａｔＧ基因ＳＳＣＰ也异常。结果表明，某些结核分枝杆菌ＩＮＨ耐药性可能是由于其ｋａｔＧ基因完全缺失、ｋａｔＧ基因或ｉｎｈＡ调节序列突变所致，但某些菌株也可能与其无关，是其它耐药基因所致或存在多种机制，尚需进一步探讨。
In order to understand the mutations of the katG gene and inhA regulatory sequences of the isoniazid-resistant (INH) isolates of Mycobacterium tuberculosis, its possible role in INH resistance was explored. The katG gene and inhA regulatory sequences of 62 clinical isolates of Mycobacterium tuberculosis were analyzed by polymerase chain reaction (PCR) and PCR-single strand conformation polymorphism (SSCP). PCR analysis showed that the sensitivity of katG gene and inhA regulatory sequence was 1 ~ 10 pg DNA; PCR amplification of its primers was highly specific. The H37Rv standard strain as a control, 13 strains of sensitive strains, 12 katG gene amplification products SSCP swimming normal, 1 katG abnormalities; 24 non-INH anti-TB drug strains, 8 katGSSCP abnormalities; 27 The inhA regulatory sequence SSCP were all normal. Among 25 isolates of INH resistance, three katG genes were negative for PCR amplification and 22 were positive for katG amplification, of which 16 were SSCP motile abnormalities. Four inhA regulatory sequences SSCP were abnormally migrated and their katG gene SSCP was also abnormal. The results showed that some M. tuberculosis INH resistance may be due to its complete deletion of katG gene, katG gene or inhA regulatory sequence mutations, but some strains may also have nothing to do with it, is caused by other drug resistance genes or exist A variety of mechanisms need to be further explored.