The genetics and biochemistry of isoniazid resistance in mycobacterium tuberculosis.

R A Slayden, C E Barry
Author Information
  1. R A Slayden: Tuberculosis Research Section, Laboratory of Host Defenses, NIAID, NIH, 12441 Parklawn Dr., Rockville 20852, USA.

Abstract

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 to INH. Despite the wealth of genetic information currently available, the molecular mechanism of cell death induced by INH remains elusive.

Grants

  1. Z01 AI000783-11/Intramural NIH HHS

MeSH Term

Antitubercular Agents
Bacterial Proteins
Drug Resistance, Microbial
Humans
Isoniazid
Mutation
Mycobacterium tuberculosis
Peroxidases
Tuberculosis, Pulmonary

Chemicals

Antitubercular Agents
Bacterial Proteins
Peroxidases
catalase HPI
Isoniazid

Word Cloud

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