Evidence map›Paper›PMID 9661035›Full record

ArticleAntimicrobial agents and chemotherapy1998

Contribution of rpoB mutations to development of rifamycin cross-resistance in Mycobacterium tuberculosis.

D L Williams, L Spring, L Collins, L P Miller, L B Heifets, P R Gangadharam, T P Gillis

Open access · bronzeAbstract read
In one paragraph

Article in Antimicrobial agents and chemotherapy, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed, 2 pooled it
3.7field-weighted citation impact, top 7% 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

98 citing papers in PubMed, 2 syntheses or guidelines pooled it, 235 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Microbiology spectrum · 2026
    Article
  5. Article
  6. Review
  7. Development and hepatotoxicity of rifamycin derivatives.Expert opinion on drug metabolism & toxicology · 2025
    Review
  8. Rapid detection of rifampin resistance inMicrobiology spectrum · 2025
    Article
  9. Review
  10. Review
  11. An Overview of Various Rifampicin Analogs againstMedicinal chemistry (Shariqah (United Arab Emirates)) · 2024
    Review
  12. Molecular Characterization and Antimicrobial Susceptibilities ofAnimals : an open access journal from MDPI · 2023
    Article
  13. Article
  14. Article
  15. Article
  16. Infection and drug resistance · 2021
    Article
  17. Article
  18. Article
  19. Article
  20. Article

38 more citing papers are in PubMed but not listed here.

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

7 authors at 5 institutions in 1 country.

D L WilliamsGillis W. Long Hansen's Disease Research Laboratory, School of Veterinary Medicine, Louisiana State University, Baton Rouge 70894, USA. dwill21@lsu.edu
L Spring
L Collins
L P Miller
L B Heifets
P R Gangadharam
T P Gillis
Louisiana State University · USNational Hansen's Disease Program · USNational Jewish Health · USRutgers, The State University of New Jersey · USUniversity of Illinois Chicago · US

Funding

DNA DIAGNOSTIC ASSAY FOR RIFAMPIN-RESISTANT TUBERCULOSISR29AI035274 · NIAID · NATIONAL HANSEN'S DISEASE PROGRAM · PI WILLIAMS, DIANA L · 1993 to 1997
–
NIAID NIH HHS AI35274
6 · The paper itself

Abstract

The contributions of 23 insertion, deletion, or missense mutations within an 81-bp fragment of rpoB, the gene encoding the beta-subunit of the DNA-dependent RNA polymerase of Mycobacterium tuberculosis, to the development of resistance to rifamycins (rifampin, rifabutin, rifapentine, and KRM-1648) in 29 rifampin-resistant clinical isolates were defined. Specific mutant rpoB alleles led to the development of cross-resistance to all rifamycins tested, while a subset of mutations were associated with resistance to rifampin and rifapentine but not to KRM-1648 or rifabutin. To further study the impact of specific rpoB mutant alleles on the development of rifamycin resistance, mutations were incorporated into the rpoB gene of M. tuberculosis H37Rv, contained on a mycobacterial shuttle plasmid, by in vitro mutagenesis. Recombinant M. tuberculosis clones containing plasmids with specific mutations in either codon 531 or 526 of rpoB exhibited high-level resistance to all rifamycins tested, whereas clones containing a plasmid with a mutation in codon 516 exhibited high-level resistance to rifampin and rifapentine but were susceptible to both rifabutin and KRM-1648. These results provided additional proof of the association of specific rpoB mutations with the development of rifamycin resistance and corroborate previous reports of the usefulness of rpoB genotyping for predicting rifamycin-resistant phenotypes.

Indexed as

MutationAnti-Bacterial AgentsBase SequenceDNA, BacterialDNA-Directed RNA PolymerasesDrug Resistance, MicrobialMolecular Sequence DataMycobacterium tuberculosisRifamycinsAnti-Bacterial AgentsDNA, BacterialDNA-Directed RNA PolymerasesRifamycinsRNA polymerase beta subunit

Identifiers

PMID9661035
PMCPMC105697
OpenAlexW2160529344

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.