Publication: Analysis of RNA polymerase gene mutation in three isolates of rifampicin resistant Mycobacterium tuberculosis.
3
item.page.dc.date.issued
1995-12-01
item.page.dc.type
item.page.dc.identifier.issn
01251562
item.page.dc.identifier.other
2-s2.0-0029442303
item.page.dc.rights
Mahidol University
item.page.dc.rights.holder
SCOPUS
item.page.dc.identifier.citation
The Southeast Asian journal of tropical medicine and public health. Vol.26 Suppl 1, (1995), 333-336
punsarn.item.page.citation
P. Vattanaviboon, R. Sukchawalit, P. Jearanaikoon, C. Chuchottaworn, M. Ponglikitmongkol Analysis of RNA polymerase gene mutation in three isolates of rifampicin resistant Mycobacterium tuberculosis.. The Southeast Asian journal of tropical medicine and public health. Vol.26 Suppl 1, (1995), 333-336. Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/17342
Research Projects
Organizational Units
Authors
Journal Issue
relationships.isThesisOf
item.page.dc.title
Analysis of RNA polymerase gene mutation in three isolates of rifampicin resistant Mycobacterium tuberculosis.
item.page.dc.contributor.author
item.page.dc.contributor.other
item.page.dc.description.abstract
Drug resistance in tuberculosis (TB) has become a major public health threat, particularly when the disease cannot be 100% controlled by BCG vaccination. In Thailand, resistance to rifampicin, a major component of multidrug regimens of treatment, is the common cause of tuberculosis recurrence. The mechanism of rifampicin resistance involves alterations of the RNA polymerase subunit beta (rpo B) gene. Mutations in rpo B gene were often found to cluster within a region of 23 amino acids starting from amino acid residue 511 to residue 533. Direct PCR sequencing was utilized to compare base changes in rpo B gene in three rifampicin resistant phenotypes of M. tuberculosis isolated from Thai patients. The sequences showed one base substitution at codon 531 resulting in an amino acid change from serine (TCG) to leucine (TTG) in a multidrug resistant isolate compared to that of a sensitive isolate, whereas a point mutation at codon 516 causing a change from aspartic acid (GAC) to tyrosine (TAC) was detected in a multidrug resistant isolate from a HIV positive patient. In an isolate resistant only to rifampicin a double mutation at codon 531 changing serine (TCG) to phenylalanine (TTT) was found. No mutations were observed in the same region in streptomycin, ethambutol or isoniazid resistant isolates. This finding reports two new types of mutation (GAC to TAC at codon 516 and TCG to TTT at codon 531) and confirms a direct correlation between rpo B gene alteration and rifampicin resistant phenotype in M. tuberculosis.