ArticleAntimicrobial agents and chemotherapy2006
Population genetics study of isoniazid resistance mutations and evolution of multidrug-resistant Mycobacterium tuberculosis.
Article in Antimicrobial agents and chemotherapy, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 168 papers, 1 of them a synthesis that pooled it.
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Who cites it
168 citing papers in PubMed, 1 synthesis or guideline pooled it, 384 citations in OpenAlex.
- GenoType MTBDRplus Assay for Rapid Detection of Multidrug Resistance in Mycobacterium tuberculosis: A Meta-Analysis.PloS one · 2016Pooled it
- Molecular Interplay of Brucellosis and Tuberculosis: Insights into Telomere Biology, Oxidative Stress, and Drug Resistance Mechanisms.Diseases (Basel, Switzerland) · 2026Review
- A new Persister Enrichment Model inbioRxiv : the preprint server for biology · 2026Article
- Predicting isoniazid resistance inJournal of clinical microbiology · 2026Article
- Uncovering the structural impact of KatG Ser315 mutations in Mycobacterium tuberculosis via cryo-EM.Protein science : a publication of the Protein Society · 2026Article
- Exploring transmission dynamics in epidemiologically linked pulmonary tuberculosis cases and household contacts: a WGS-based investigation.BMC genomics · 2025Article
- Evaluating selection at intermediate scales within genes provides robust identification of genes under positive selection in M. tuberculosis clinical isolates.Tuberculosis (Edinburgh, Scotland) · 2025Article
- Evaluating selection at intermediate scales within genes provides robust identification of genes under positive selection inbioRxiv : the preprint server for biology · 2025Article
- Fitness Effect of the Isoniazid Resistance Mutation S315T of the Catalase-Peroxidase Enzyme KatG of Mycobacterium tuberculosis.Genome biology and evolution · 2025Article
- The power of DNA-encoded chemical libraries in the battle against drug-resistant bacteria.RSC advances · 2025Review
- Comprehensive analysis of mutations associated with rifampicin- and isoniazid-resistant tuberculosis in a high-burden setting.Revista da Sociedade Brasileira de Medicina Tropical · 2025Article
- Feature selection and aggregation for antibiotic resistance GWAS inFrontiers in microbiology · 2025Article
- Article
- Country-level heterogeneity in MDR-TB drug susceptibility supports country-specific policy development.Frontiers in tuberculosis · 2025Article
- Article
- Differential Host Gene Expression in Response to Infection by DifferentMicroorganisms · 2024Article
- Exploring gene mutations and multidrug resistance in Mycobacterium tuberculosis: a study from the Lung Hospital in Vietnam.Molecular biology reports · 2024Article
- L-DNA-Based Melt Analysis Enables Within-Sample Validation of PCR Products.Analytical chemistry · 2024Article
- Combating antimicrobial resistance in malaria, HIV and tuberculosis.Nature reviews. Drug discovery · 2024Review
- An HLA-E-targeted TCR bispecific molecule redirects T cell immunity against Mycobacterium tuberculosis.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
108 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
19 authors at 13 institutions in 6 countries.
Funding
Abstract
The molecular basis for isoniazid resistance in Mycobacterium tuberculosis is complex. Putative isoniazid resistance mutations have been identified in katG, ahpC, inhA, kasA, and ndh. However, small sample sizes and related potential biases in sample selection have precluded the development of statistically valid and significant population genetic analyses of clinical isoniazid resistance. We present the first large-scale analysis of 240 alleles previously associated with isoniazid resistance in a diverse set of 608 isoniazid-susceptible and 403 isoniazid-resistant clinical M. tuberculosis isolates. We detected 12 mutant alleles in isoniazid-susceptible isolates, suggesting that these alleles are not involved in isoniazid resistance. However, mutations in katG, ahpC, and inhA were strongly associated with isoniazid resistance, while kasA mutations were associated with isoniazid susceptibility. Remarkably, the distribution of isoniazid resistance-associated mutations was different in isoniazid-monoresistant isolates from that in multidrug-resistant isolates, with significantly fewer isoniazid resistance mutations in the isoniazid-monoresistant group. Mutations in katG315 were significantly more common in the multidrug-resistant isolates. Conversely, mutations in the inhA promoter were significantly more common in isoniazid-monoresistant isolates. We tested for interactions among mutations and resistance to different drugs. Mutations in katG, ahpC, and inhA were associated with rifampin resistance, but only katG315 mutations were associated with ethambutol resistance. There was also a significant inverse association between katG315 mutations and mutations in ahpC or inhA and between mutations in kasA and mutations in ahpC. Our results suggest that isoniazid resistance and the evolution of multidrug-resistant strains are complex dynamic processes that may be influenced by interactions between genes and drug-resistant phenotypes.
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