ArticleBMC genomics2024
Identification of novel single nucleotide variants in the drug resistance mechanism of Mycobacterium tuberculosis isolates by whole-genome analysis.
Article in BMC genomics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Sequence-encoded determinants of regional mutational plasticity: comparative analysis of PE_PGRS genes in Mycobacterium tuberculosis and other bacteria.Scientific reports · 2026Article
- High-Quality Genome Assemblies of Two Prototheca wickerhamii Strains.Scientific data · 2026Article
- Genomic landscape ofNew microbes and new infections · 2025Article
- Article
- sRNAdeep: a novel tool for bacterial sRNA prediction based on DistilBERT encoding mode and deep learning algorithms.BMC genomics · 2024Article
- Phenotypic and genotypic perspectives on detection methods for bacterial antimicrobial resistance in a One Health context: research progress and prospects.Archives of microbiology · 2024Review
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Authors and funding
7 authors.
Funding
Abstract
backgroundTuberculosis (TB) represents a major global health challenge. Drug resistance in Mycobacterium tuberculosis (MTB) poses a substantial obstacle to effective TB treatment. Identifying genomic mutations in MTB isolates holds promise for unraveling the underlying mechanisms of drug resistance in this bacterium.
methodsIn this study, we investigated the roles of single nucleotide variants (SNVs) in MTB isolates resistant to four antibiotics (moxifloxacin, ofloxacin, amikacin, and capreomycin) through whole-genome analysis. We identified the drug-resistance-associated SNVs by comparing the genomes of MTB isolates with reference genomes using the MuMmer4 tool.
resultsWe observed a strikingly high proportion (94.2%) of MTB isolates resistant to ofloxacin, underscoring the current prevalence of drug resistance in MTB. An average of 3529 SNVs were detected in a single ofloxacin-resistant isolate, indicating a mutation rate of approximately 0.08% under the selective pressure of ofloxacin exposure. We identified a set of 60 SNVs associated with extensively drug-resistant tuberculosis (XDR-TB), among which 42 SNVs were non-synonymous mutations located in the coding regions of nine key genes (ctpI, desA3, mce1R, moeB1, ndhA, PE_PGRS4, PPE18, rpsA, secF). Protein structure modeling revealed that SNVs of three genes (PE_PGRS4, desA3, secF) are close to the critical catalytic active sites in the three-dimensional structure of the coding proteins.
conclusionThis comprehensive study elucidates novel resistance mechanisms in MTB against antibiotics, paving the way for future design and development of anti-tuberculosis drugs.
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