Evidence map›Paper›PMID 24055765›Full record

SynthesisThe Journal of antimicrobial chemotherapy2014

Systematic review of allelic exchange experiments aimed at identifying mutations that confer drug resistance in Mycobacterium tuberculosis.

Hanna Nebenzahl-Guimaraes, Karen R Jacobson, Maha R Farhat, Megan B Murray

Open access · bronzeAbstract readSystematic Review
In one paragraph

Synthesis in The Journal of antimicrobial chemotherapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
5.6field-weighted citation impact, top 3% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 92 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Prevalence ofJournal of clinical tuberculosis and other mycobacterial diseases · 2023
    Article
  10. Article
  11. Article
  12. Globally diverseThe Lancet. Microbe · 2021
    Article
  13. Article
  14. Infection and drug resistance · 2021
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 4 institutions in 5 countries.

Hanna Nebenzahl-GuimaraesDepartment of Epidemiology, Harvard School of Public Health, Boston, MA 02115, USA.
Karen R Jacobson
Maha R Farhat
Megan B Murray
Centre For Human Genetics · INHarvard Global Health Institute · USMassachusetts General Hospital · USNational Institute for Public Health and the Environment · NL

Funding

Geospatial clustering and molecular and social epidemiology of drug resistant TBK01TW009213 · FIC · MASSACHUSETTS GENERAL HOSPITAL · PI JACOBSON, KAREN R · 2011 to 2015
$715k
FIC NIH HHS K01 TW009213Intramural NIH HHSPHS HHS U19 A1076217
6 · The paper itself

Abstract

backgroundImproving our understanding of the relationship between the genotype and the drug resistance phenotype of Mycobacterium tuberculosis will aid the development of more accurate molecular diagnostics for drug-resistant tuberculosis. Studies that use direct genetic manipulation to identify the mutations that cause M. tuberculosis drug resistance are superior to associational studies in elucidating an individual mutation's contribution to the drug resistance phenotype.

methodsWe systematically reviewed the literature for publications reporting allelic exchange experiments in any of the resistance-associated M. tuberculosis genes. We included studies that introduced single point mutations using specialized linkage transduction or site-directed/in vitro mutagenesis and documented a change in the resistance phenotype.

resultsWe summarize evidence supporting the causal relationship of 54 different mutations in eight genes (katG, inhA, kasA, embB, embC, rpoB, gyrA and gyrB) and one intergenic region (furA-katG) with resistance to isoniazid, the rifamycins, ethambutol and fluoroquinolones. We observed a significant role for the strain genomic background in modulating the resistance phenotype of 21 of these mutations and found examples of where the same drug resistance mutations caused varying levels of resistance to different members of the same drug class.

conclusionsThis systematic review highlights those mutations that have been shown to causally change phenotypic resistance in M. tuberculosis and brings attention to a notable lack of allelic exchange data for several of the genes known to be associated with drug resistance.

Indexed as

AllelesAnimalsAntitubercular AgentsHumansMutationMycobacterium tuberculosisTuberculosis, Multidrug-ResistantAntitubercular Agentsgeneticsin vitro resistancemicrobial susceptibility testsM. tuberculosisSNPs

Identifiers

PMID24055765
PMCPMC3886931
OpenAlexW2104818573

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.