Exclusive mutations related to isoniazid and ethionamide resistance among Mycobacterium tuberculosis isolates from Korea
OBJECTIVE: To understand the molecular basis for M. tuberculosis resistance to INH and ETH.
DESIGN: The sequence polymorphism at the 94th codon of inhA among M. tuberculosis isolates from Korea was analyzed by polymerase chain reaction (PCR) cloning and sequence analysis.
RESULTS: No nucleotide change at the 94th codon of inhA was detected in any of the 24 INH-resistant isolates analyzed in this study. On the other hand, a point mutation was found exclusively at the regulatory region flanking a putative ribosome-binding site of the inhA locus in 14 isolates. Interestingly, all the mutations were of the same kind, which substitutes C to T. Among 14 isolates, 12 were resistant to INH as well as to ETH, while two were resistant to INH only.
DISCUSSION: It seems that mutations previously found at the 94th codon of inhA have no particular relationship with the mechanism involved in the resistance of M. tuberculosis to INH and/or ETH. On the other hand, the resistance mechanism of M. tuberculosis to INH/ETH may involve an altered level of inhA, an expression which may have been influenced by the sequence change in the regulatory region of the inhA locus.
Document Type: Regular Paper
Affiliations: 1: Korean Institute of Tuberculosis, The Korean National Tuberculosis Association, Seoul, Korea; and Institute for Immunology and Immunological Diseases, Seoul, Korea 2: Institute for Immunology and Immunological Diseases, Seoul, Korea; and Department of Microbiology, Yonsei University College of Medicine, Seoul, Korea 3: Korean Institute of Tuberculosis, The Korean National Tuberculosis Association, Seoul, Korea
Publication date: 2000-05-01
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