ReviewClinical microbiology reviews2006
Tuberculosis chemotherapy: the influence of bacillary stress and damage response pathways on drug efficacy.
Review in Clinical microbiology reviews, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
71 citing papers in PubMed, 1 synthesis or guideline pooled it, 141 citations in OpenAlex.
- Identification of gene targets against dormant phase Mycobacterium tuberculosis infections.BMC infectious diseases · 2007Pooled it
- Fluctuating environmental adaptation shapes antibiotic survival in Mycobacterium tuberculosis.Journal of microbiology (Seoul, Korea) · 2026Article
- How macrophage heterogeneity affects tuberculosis disease and therapy.Nature reviews. Immunology · 2025Review
- MtrA modulates Mycobacterium tuberculosis cell division in host microenvironments to mediate intrinsic resistance and drug tolerance.Cell reports · 2023Article
- Spatiotemporal perspectives on tuberculosis chemotherapy.Current opinion in microbiology · 2023Review
- Sulforaphane kills Mycobacterium tuberculosis H37Ra and Mycobacterium smegmatis mcJournal of microbiology (Seoul, Korea) · 2022Article
- Label-free affinity screening, design and synthesis of inhibitors targeting the Mycobacterium tuberculosis L-alanine dehydrogenase.PloS one · 2022Article
- Are all antibiotic persisters created equal?Frontiers in cellular and infection microbiology · 2022Review
- Division of labor between SOS and PafBC in mycobacterial DNA repair and mutagenesis.Nucleic acids research · 2021Article
- Systematic measurement of combination-drug landscapes to predict in vivo treatment outcomes for tuberculosis.Cell systems · 2021Article
- Flow cytometry method for absolute counting and single-cell phenotyping of mycobacteria.Scientific reports · 2021Article
- Transcriptional regulator-induced phenotype screen reveals drug potentiators in Mycobacterium tuberculosis.Nature microbiology · 2021Article
- Revisiting the methods for detectingAccess microbiology · 2021Review
- Evolution of Drug-ResistantFrontiers in microbiology · 2021Review
- Rapidly Correcting Frameshift Mutations in the Mycobacterium tuberculosisAntimicrobial agents and chemotherapy · 2020Article
- Digital Image Analysis of Heterogeneous Tuberculosis Pulmonary Pathology in Non-Clinical Animal Models using Deep Convolutional Neural Networks.Scientific reports · 2020Article
- Comprehensive analysis of protein acetyltransferases of human pathogen Mycobacterium tuberculosis.Bioscience reports · 2019Article
- Phase variation inProceedings of the National Academy of Sciences of the United States of America · 2019Article
- Harnessing Biological Insight to Accelerate Tuberculosis Drug Discovery.Accounts of chemical research · 2019Review
- Competing evolutionary paths in growing populations with applications to multidrug resistance.PLoS computational biology · 2019Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The global tuberculosis (TB) control effort is focused on interrupting transmission of the causative agent, Mycobacterium tuberculosis, through chemotherapeutic intervention in active infectious disease. The insufficiency of this approach is manifest in the inexorable annual increase in TB infection and mortality rates and the emergence of multidrug-resistant isolates. Critically, the limited efficacy of the current frontline anti-TB drug combination suggests that heterogeneity of host and bacillary physiologies might impair drug activity. This review explores the possibility that strategies enabling adaptation of M. tuberculosis to hostile in vivo conditions might contribute to the subversion of anti-TB chemotherapy. In particular, evidence that infecting bacilli are exposed to environmental and host immune-mediated DNA-damaging insults suggests a role for error-prone DNA repair synthesis in the generation of chromosomally encoded antibiotic resistance mutations. The failure of frontline anti-TB drugs to sterilize a population of susceptible bacilli is independent of genetic resistance, however, and instead implies the operation of alternative tolerance mechanisms. Specifically, it is proposed that the emergence of persister subpopulations might depend on the switch to an altered metabolic state mediated by the stringent response alarmone, (p)ppGpp, possibly involving some or all of the many toxin-antitoxin modules identified in the M. tuberculosis genome.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.