Evidence map›Paper›PMID 28343421›Full record

ArticleFuture microbiology2017

In vitro and in vivo fitness costs associated with Mycobacterium tuberculosis RpoB mutation H526D.

Dalin Rifat, Victoria L Campodónico, Jing Tao, James A Miller, Alpaslan Alp, Yufeng Yao, Petros C Karakousis

Abstract read
In one paragraph

Article in Future microbiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

  1. Discordance between genotypic and phenotypic methods for the detection of rifampicin and isoniazid resistantJournal of clinical tuberculosis and other mycobacterial diseases · 2024
    Article
  2. Article
  3. Mutations inmBio · 2023
    Article
  4. Article
  5. Environmental Dependence of Competitive Fitness in Rifampin-ResistantApplied and environmental microbiology · 2022
    Article
  6. Resistance-Conferring Mycobacterial Mutations and Quantification of Early Bactericidal Activity.American journal of respiratory and critical care medicine · 2021
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Identification of Genetic Features for Attenuation of TwoFrontiers in veterinary science · 2019
    Article
  13. Article
  14. AlteredFrontiers in microbiology · 2018
    Article
  15. 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

7 authors.

Dalin RifatDepartment of Medicine, Johns Hopkins University School of Medicine, Baltimore MD 21287, USA.
Victoria L CampodónicoDepartment of Medicine, Johns Hopkins University School of Medicine, Baltimore MD 21287, USA.
Jing TaoDepartment of Medicine, Johns Hopkins University School of Medicine, Baltimore MD 21287, USA.
James A MillerDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore MD 21287, USA.
Alpaslan AlpDepartment of Medicine, Johns Hopkins University School of Medicine, Baltimore MD 21287, USA.
Yufeng YaoDepartment of Microbiology & Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Petros C KarakousisDepartment of Medicine, Johns Hopkins University School of Medicine, Baltimore MD 21287, USA.

Funding

The Role of Cell Wall Lipids in Pathogenesis of Rifampin-Resistant TBR01AI106613 · NIAID · JOHNS HOPKINS UNIVERSITY · PI KARAKOUSIS, PETROS C · 2013 to 2015
$765k
NIAID NIH HHS R01 AI106613
6 · The paper itself

Abstract

aimThere is controversy regarding the potential fitness costs of rifampicin (RIF) resistance-conferring mutations in the Mycobacterium tuberculosis (Mtb) rpoB gene. We characterized the pathogenicity of an Mtb RpoB H526D mutant. MATERIALS &

methodsA mutant containing the RpoB H526D mutation was isolated from wild-type Mtb grown on RIF-containing plates and complemented for determination of in vitro and in vivo fitness costs.

resultsThe RpoB H526D mutant showed reduced survival relative to control strains during progressive hypoxia and delayed growth following resuscitation from nutrient starvation (p < 0.05), which was associated with reduced expression of the resuscitation-promoting factor genes rpfB, rpfC and rpfE. Relative to the isogenic wild-type strain, the mutant showed significantly attenuated growth and long-term survival as well as reduced inflammation in mouse lungs. Conclusion & future perspective: Our data suggest that RpoB H526D mutation confers a fitness cost during growth-limiting conditions in vitro and in mouse lungs.

Indexed as

Genetic FitnessMutationAnimalsAntitubercular AgentsBacterial ProteinsDisease Models, AnimalDNA-Directed RNA PolymerasesDrug Resistance, BacterialGenetic Complementation TestHumansInflammationLungMiceMicrobial Sensitivity TestsMicrobial ViabilityMycobacterium tuberculosisAntitubercular AgentsBacterial ProteinsDNA-Directed RNA PolymerasesOxygenrpoB protein, Mycobacterium tuberculosisinflammationmurine modelMycobacterium tuberculosisnutrient starvationpersistenceprogressive hypoxiaresuscitation-promoting factorRpfrpoBstringent responsevirulence

Identifiers

PMID28343421
PMCPMC5506874

What OpenQuestion holds

Textmetadata
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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.