The genetics and biochemistry of isoniazid resistance in Mycobacterium tuberculosis

被引：161
作者：
Slayden, RA [1 ]
Barry, CE [1 ]
机构：
[1] NIAID, TB Res Sect, Host Def Lab, NIH, Rockville, MD 20852 USA
来源：
MICROBES AND INFECTION | 2000年 / 2卷 / 06期
关键词：
isoniazid; KatG; catalase; tuberculosis; pro-drug;
D O I：
10.1016/S1286-4579(00)00359-2
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
Although the primary targets of activated isoniazid (INH) are proteins involved in the biosynthesis of cell wall mycolic acids, clinical resistance is dominated by specific point mutations in katG. Mutations associated with target mutations contribute to, but still cannot completely explain, resistance ro INH. Despite the wealth of genetic information currently available, the molecular mechanism of cell death induced by INH remains elusive. (C) 2000 Editions scientifiques et medicales Elsevier SAS.
引用
收藏
页码：659 / 669
页数：11
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