ArticleNature communications2023
The evolution of antibiotic resistance is associated with collateral drug phenotypes in Mycobacterium tuberculosis.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 67 citations in OpenAlex.
- Mutations in RNA polymerase that drive the emergence of antibiotic resistance.Current opinion in microbiology · 2026Review
- Heterogeneity in microbial antibiotic responses: genetic basis and within-host evolution.Trends in genetics : TIG · 2026Review
- Genome scale CRISPRi reveals both shared and strain-specific vulnerabilities in genetically diverse drug-resistant strains of Mycobacterium tuberculosis.Nature communications · 2026Article
- A functional amyloid matrix underpins the PDIM-architected corded superstructure of thebioRxiv : the preprint server for biology · 2026Article
- Uncovering resistance pathways to first- and last-line antibiotics inMicrobial genomics · 2026Article
- Menaquinone depletion resensitises bedaquiline-resistant tuberculosis.bioRxiv : the preprint server for biology · 2026Article
- Vγ9Vδ2 T cells in tuberculosis: protective immunity and translational perspectives.Frontiers in immunology · 2026Review
- Verapamil Suppresses the Development of Resistance Against Anti-Tuberculosis Drugs in Mycobacteria.International journal of molecular sciences · 2025Article
- Article
- Selective silencing of antibiotic-tethered ribosomes as a resistance mechanism against aminoglycosides.Nature communications · 2025Article
- Genetic determinants ofMicrobiology spectrum · 2025Article
- Collateral sensitivity and cross-resistance in six species of bacteria exposed to six classes of antibiotics.Microbiology spectrum · 2025Article
- Study on collateral sensitivity of tigecycline to colistin-resistantMicrobiology spectrum · 2025Article
- Strategies for shortening tuberculosis therapy.Nature medicine · 2025Review
- Structure and assembly of the MmpL5/MmpS5 efflux transporter from Mycobacterium tuberculosis.Nature communications · 2025Article
- Verapamil and its metabolite norverapamil inhibit theProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Genetic and Cheminformatic Characterization ofACS infectious diseases · 2025Article
- Enhanced diagnosis of multi-drug-resistant microbes using group association modeling and machine learning.Nature communications · 2025Article
- A mutation in RNA polymerase imparts resistance to β-lactams by preventing dysregulation of amino acid and nucleotide metabolism.Cell reports · 2025Article
- Functions of nitroreductases in mycobacterial physiology and drug susceptibility.Journal of bacteriology · 2025Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The increasing incidence of drug resistance in Mycobacterium tuberculosis has diminished the efficacy of almost all available antibiotics, complicating efforts to combat the spread of this global health burden. Alongside the development of new drugs, optimised drug combinations are needed to improve treatment success and prevent the further spread of antibiotic resistance. Typically, antibiotic resistance leads to reduced sensitivity, yet in some cases the evolution of drug resistance can lead to enhanced sensitivity to unrelated drugs. This phenomenon of collateral sensitivity is largely unexplored in M. tuberculosis but has the potential to identify alternative therapeutic strategies to combat drug-resistant strains that are unresponsive to current treatments. Here, by using drug susceptibility profiling, genomics and evolutionary studies we provide evidence for the existence of collateral drug sensitivities in an isogenic collection M. tuberculosis drug-resistant strains. Furthermore, in proof-of-concept studies, we demonstrate how collateral drug phenotypes can be exploited to select against and prevent the emergence of drug-resistant strains. This study highlights that the evolution of drug resistance in M. tuberculosis leads to collateral drug responses that can be exploited to design improved drug regimens.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.