The genetics and biochemistry of isoniazid resistance in Mycobacterium tuberculosis

Citation
Ra. Slayden et Ce. Barry, The genetics and biochemistry of isoniazid resistance in Mycobacterium tuberculosis, MICROBES IN, 2(6), 2000, pp. 659-669
Citations number
109
Categorie Soggetti
Immunology
Journal title
MICROBES AND INFECTION
ISSN journal
12864579 → ACNP
Volume
2
Issue
6
Year of publication
2000
Pages
659 - 669
Database
ISI
SICI code
1286-4579(200005)2:6<659:TGABOI>2.0.ZU;2-S
Abstract
Although the primary targets of activated isoniazid (INH) are proteins invo lved in the biosynthesis of cell wall mycolic acids, clinical resistance is dominated by specific point mutations in katG. Mutations associated with t arget mutations contribute to, but still cannot completely explain, resista nce ro INH. Despite the wealth of genetic information currently available, the molecular mechanism of cell death induced by INH remains elusive. (C) 2 000 Editions scientifiques et medicales Elsevier SAS.