Mutations in the beginning of the rpoB gene can induce resistance to rifamycins in both Helicobacter pylori and Mycobacterium tuberculosis.
A clinical isolate of Helicobacter pylori that developed resistance to rifabutin during therapy carried an rpoB gene that retained a wild-type cluster region sequence but had acquired a novel codon 149 (V149F) mutation. In transformation experiments, the mutation was shown to confer high-level rifabutin resistance. The equivalent mutation (V176F) was present in several resistant isolates of Mycobacterium tuberculosis.
Heep
M
M
Institute for Medical Microbiology, Regensburg, Germany. Markus.Heep@klinik.uni-regensburg.de
Rieger
U
U
Beck
D
D
Lehn
N
N
D000595:Amino Acid Sequence; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D003062:Codon; D012321:DNA-Directed RNA Polymerases / Q000235:genetics*; D004351:Drug Resistance; D016480:Helicobacter pylori / Q000187:drug effects* / Q000235:genetics; D008969:Molecular Sequence Data; D009154:Mutation / Q000235:genetics; D009169:Mycobacterium tuberculosis / Q000187:drug effects* / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012294:Rifamycins / Q000494:pharmacology*
D000900:Anti-Bacterial Agents; D003062:Codon; D012294:Rifamycins; D012321:DNA-Directed RNA Polymerases; C105078:RNA polymerase beta subunit