Loss-of-function mutations in ndh do not confer delamanid, ethionamide, isoniazid, or pretomanid resistance in Mycobacterium tuberculosis

Sushil Pandey, Catherine Vilchèze, Jim Werngren, Arnold Bainomugisa, Mikael Mansjö, Ramona Groenheit, Paolo Miotto, Daniela M. Cirillo, Christopher Coulter, Alain R. Baulard, Thomas Schön, William R. Jacobs, Kamel Djaout, Claudio U. Köser

Research output: Contribution to journalArticlepeer-review

Abstract

Results from clinical strains and knockouts of the H37Rv and CDC1551 laboratory strains demonstrated that ndh (Rv1854c) is not a resistance-conferring gene for isoniazid, ethionamide, delamanid, or pretomanid in Mycobacterium tuberculosis. This difference in the susceptibility to NAD-adduct-forming drugs compared with other mycobacteria may be driven by differences in the absolute intrabacterial NADH concentration.

Original languageEnglish (US)
JournalAntimicrobial agents and chemotherapy
Volume68
Issue number1
DOIs
StatePublished - Jan 2024

Keywords

  • Mycobacterium tuberculosis
  • delamanid
  • ethionamide
  • isoniazid
  • pretomanid

ASJC Scopus subject areas

  • Pharmacology
  • Pharmacology (medical)
  • Infectious Diseases

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