Evidence map›Paper›PMID 19146699›Full record

ArticleBMC microbiology2009

Genetic evaluation of relationship between mutations in rpoB and resistance of Mycobacterium tuberculosis to rifampin.

Anna Zaczek, Anna Brzostek, Ewa Augustynowicz-Kopec, Zofia Zwolska, Jaroslaw Dziadek

Open access · goldAbstract read
In one paragraph

Article in BMC microbiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 12% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.

  1. Pooled it
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  6. Tuberculosis challenges: Resistance, co-infection, diagnosis, and treatment.European journal of microbiology & immunology · 2022
    Review
  7. Article
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  10. Mutations Associated with Rifampicin Resistance inInterdisciplinary perspectives on infectious diseases · 2020
    Review
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  15. Comparison of TaqMan(®) Array Card and MYCOTB(TM) with conventional phenotypic susceptibility testing in MDR-TB.The international journal of tuberculosis and lung disease : the official journal of the International Union against Tuberculosis and Lung Disease · 2016
    Article
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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

5 authors at 3 institutions in 1 country.

Anna ZaczekInstitute for Medical Biology, Polish Academy of Sciences, Lodz, Poland. ania.zaczek@yahoo.pl
Anna Brzostek
Ewa Augustynowicz-Kopec
Zofia Zwolska
Jaroslaw Dziadek
Institute for Medical Biology · PLNational Institute of Public Health · PLPolish Academy of Sciences · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRifampin is a first line antituberculosis drug active against bacilli in logarithmic and stationary phase, which interferes with RNA synthesis by binding to bacterial RNA polymerase. Tubercle bacilli achieve resistance to rifampin by accumulation of mutations in a short-81 bp region of the rpoB gene. Among many mutations identified in the rpoB gene, few were verified by molecular genetic methods as responsible for resistance to rifampin (RMP).

resultsIn this study eight different mutations identified in an 81 bp section of a "hot spot" region of the rpoB gene of RMP resistant Mycobacterium tuberculosis clinical strains were evaluated in respect to drug resistance. It was found that: mutations in positions 526 (H/D), 516 (D/V) and 531 (S/L) result in high level resistance to rifampin; mutations in positions 516 (D/Y), 515 (M/I), 510 (Q/H) or a double mutation in codons 512 (S/I) and 516 (D/G) relate to low level of resistance. Gene rpoB carrying mutations in codon 513 (Q/L) introduced into an M. tuberculosis laboratory strain did not cause resistance to rifampin, however the same gene introduced into two different clinical strains did, with the level of resistance depending on the host strain.

conclusionMutations in an 81 bp "hot spot" region of the rpoB of M. tuberculosis lead to different levels of resistance to rifampin. Some mutations in this "hot spot" region of rpoB require a specific genetic background for the host strain to develop resistance to rifampin. Therefore, the identification of such mutations in a clinical M. tuberculosis strain is not enough to classify the given strain as resistant to rifampin.

Indexed as

Amino Acid SubstitutionAntitubercular AgentsBacterial ProteinsDNA, BacterialDNA-Directed RNA PolymerasesDrug Resistance, BacterialMicrobial Sensitivity TestsModels, GeneticMutationMycobacterium tuberculosisRifampinAntitubercular AgentsBacterial ProteinsDNA, BacterialDNA-Directed RNA PolymerasesRifampinrpoB protein, Mycobacterium tuberculosis

Identifiers

PMID19146699
PMCPMC2652454
OpenAlexW2165854405

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.