Evidence map›Paper›PMID 35366177›Full record

ArticleMolecular biology reports2022

Detection and characterization of mutations in genes related to isoniazid resistance in Mycobacterium tuberculosis clinical isolates from Iran.

Pejman Bakhtiyariniya, Azar Dokht Khosravi, Mohammad Hashemzadeh, Mohammad Savari

Open access · hybridAbstract read
In one paragraph

Article in Molecular biology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 10% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
  2. Predicting isoniazid resistance inJournal of clinical microbiology · 2026
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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

4 authors at 1 institution in 1 country.

Pejman BakhtiyariniyaInfectious and Tropical Diseases Research Center, Health Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Azar Dokht KhosraviInfectious and Tropical Diseases Research Center, Health Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. azarkhosravi69@gmail.com.ORCID http://orcid.org/0000-0002-7852-6868
Mohammad HashemzadehInfectious and Tropical Diseases Research Center, Health Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Mohammad SavariInfectious and Tropical Diseases Research Center, Health Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Ahvaz Jundishapur University of Medical Sciences · IR

Funding

Ahvaz Jundishapur University of Medical Sciences OG-9930
6 · The paper itself

Abstract

backgroundThe global rise in drug-resistant Mycobacterium tuberculosis (M.tb), and especially the significant prevalence of isoniazid (INH)-resistance constitute a significant challenge to global health. Therefore, the present study aimed to investigate mutations in prevalent gene loci-involved in INH-resistance phenotype-among M.tb clinical isolates from southwestern Iran.

methodsDrug susceptibility testing (DST) was performed using the conventional proportional method on confirmed 6620 M.tb clinical isolates, and in total, 15 INH-resistant and 18 INH-susceptible isolates were included in the study. Fragments of six genetic loci most related to INH-resistance (katG, inhA promoter, furA, kasA, ndh, oxyR-ahpC intergenic region) were PCR-amplified and sequenced. Mutations were explored by pairwise alignment with the M.tb H37Rv genome.

resultsThe analysis of gene loci revealed 13 distinct mutations in INH-resistant isolates. 60% (n = 9) of the INH-resistant isolates had mutations in katG, with codon 315 predominately (53.3%, n = 8). Mutation at InhA - 15 was found in 20% (n = 3) of resistant isolates. 26.7% (n = 4) of the INH-resistant isolates had kasA mutations, of which G269S substitution was the most common (20%, n = 3). The percentage of mutations in furA, oxyR-ahpC and ndh was 6.7% (n = 1), 46.7% (n = 7), and 20% (n = 3), respectively. Of the mutations detected in ndh and oxyR-ahpC, 5 were also observed in INH-susceptible isolates. This study revealed seven novel mutations, four of which were exclusively in resistant isolates.

conclusionsThis study supports the usefulness of katG and inhA mutations as a predictive molecular marker for INH resistance. Co-detection of katG S315 and inhA-15 mutations identified 73.3% (11 out of 15 isolates) of INH-resistant isolates.

Indexed as

Mycobacterium tuberculosisTuberculosis, Multidrug-ResistantAntitubercular AgentsBacterial ProteinsCatalaseGenes, BacterialHumansIranIsoniazidMicrobial Sensitivity TestsMutationAntitubercular AgentsBacterial ProteinsCatalaseIsoniazidfurAinhAIranIsoniazid resistancekasAkatGMycobacterium tuberculosisndhoxyR-ahpC

Identifiers

PMID35366177
PMCPMC8976162
OpenAlexW4225856057

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Registered trials

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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.