Loss-of-function mutations in ndh do not confer delamanid, ethionamide, isoniazid, or pretomanid resistance in Mycobacterium tuberculosis 2024 (English)In: Antimicrobial Agents and Chemotherapy, ISSN 0066-4804, E-ISSN 1098-6596, Vol. 68, no 1, article id e0109623Article in journal (Refereed) Published

Abstract [en]

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.

Place, publisher, year, edition, pages

AMER SOC MICROBIOLOGY , 2024. Vol. 68, no 1, article id e0109623

Keywords [en]

Mycobacterium tuberculosis; delamanid; ethionamide; isoniazid; pretomanid

National Category

Microbiology

Identifiers

URN: urn:nbn:se:liu:diva-200671DOI: 10.1128/aac.01096-23ISI: 001139943000011PubMedID: 38038476OAI: oai:DiVA.org:liu-200671DiVA, id: diva2:1834973

Note

Funding Agencies|National Institute of Health Grant [ANR-20-PAMR-0005]; PNG National Tuberculosis Programme [AI26170]; National Institute of Health

Available from: 2024-02-06 Created: 2024-02-06 Last updated: 2025-02-05

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Schön, Thomas

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Division of Inflammation and InfectionFaculty of Medicine and Health SciencesDepartment of Infectious Diseases

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Microbiology

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