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Updated: Jun 19, 2026
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System for Efficacy and Cytotoxicity Screening of Inhibitors Targeting Intracellular Mycobacterium tuberculosis
Published on: April 5, 2017
First documentation of isoniazid reversion in Mycobacterium tuberculosis
E T Richardson1, S-Y G Lin, B A Pinsky
1Department of Pathology, Stanford University School of Medicine, Stanford, California, USA.
Summary
Drug-resistant tuberculosis strains can revert to drug-susceptible in the absence of isoniazid pressure. This reversion, linked to the katG gene, may impact treatment strategies for resistant tuberculosis.
Area of Science:
- Microbiology
- Genetics
- Infectious Diseases
Background:
- Rising global prevalence of drug-resistant Mycobacterium tuberculosis strains presents a significant public health challenge.
- The stability of drug-resistant mutations in Mycobacterium tuberculosis populations under varying selective pressures remains an area of active investigation.
Observation:
- This study documented isoniazid (INH) resistance reversion in a patient with multidrug-resistant tuberculosis (TB).
- Genotypic and phenotypic analyses revealed an isogenic M. tuberculosis strain transitioned from INH-resistant to INH-susceptible phenotype without INH therapy.
Findings:
- The reversion was genetically mapped to the katG gene, specifically codon 300, reverting from a GGG (glycine) to a wild-type TGG (tryptophan) codon.
- The reconstructed mutant (H37Rv DeltakatG::katG W300G) exhibited INH resistance alongside a compromised ability to manage oxidative stress, suggesting a fitness cost associated with reversion.
Implications:
- Confirms that isoniazid-resistant mutants can revert to susceptibility when drug pressure is removed.
- Findings suggest potential implications for the clinical management of INH-resistant TB and the effective duration of isoniazid therapy.
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