The Mycobacterium tuberculosis complex (MTBC) includes M. tuberculosis (M. tb), the primary cause of human tuberculosis, M. bovis, the classical zo...

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The Mycobacterium tuberculosis complex (MTBC) is a group of bacteria causing tuberculosis (TB) in humans and animals. Understanding MTBC genetic diversity is crucial for insights into its adaptation a...

Mycobacterium tuberculosis complex (MTBC) lineages show substantial variability in virulence, but the epidemiological consequences of this variability…

YouTube video by Man Carrying Thing

Here the authors train multivariate logistic regression models on over 52,000 MTBC isolates to associate binary resistance phenotypes for 15 antitubercular drugs with variants extracted from candidate...

Genome classificator using machine learning and SNP markers. - PathoGenOmics-Lab/pathotypr

Tuberculosis (TB) is a respiratory infection that is caused by a phylogenetically related group of species known as the Mycobacterium tuberculosis complex (MTBC). Members of this complex include Mycob...

This study showed that four Mycobacterium tuberculosis complex (MTBC) sub-lineages might be introduced into China 1000–400 years ago via Europe-China dispersal routes, where they diversified into loc...

Tuberculosis (TB) is the leading cause of death from an infectious disease worldwide. Mutations arising in Mycobacterium tuberculosis complex (MTBC) strains during TB infection provide a record of bacterial adaptations, such as those needed to survive the attack of the immune system and antibiotic therapies.MethodsWe conducted a meta-analysis of MTBC sequenced strains with multiple isolates from the same patient, sourced from published studies and TB Portals. We applied a convergent evolution approach to identify heavily mutated MTBC loci across patients and estimated the rates of drug resistance (DR) acquisition during treatment.ResultsUsing 5882 high-quality genomes from 1044 patients with TB, we identified 21 genes, 25 operons, and 27 promoter regions statistically enriched by mutations compared with the rest of the genome, and additional loci with established and plausible adaptive roles approaching statistical significance. Significantly, these included multiple loci known to be involved in resistance to first-, second-, and last-line anti-TB drugs. Previously reported candidate drug-resistance and -tolerance genes (prpR, Rv2571c, fadD11, helY, ndhA, Rv0139, fadE5, bioF2, and mce1 operon) were also identified. Genes encoding regulators (phoR, whiB6, and mycP1) and effectors (espK and eccE1) of the virulence ESX-1 locus were frequently mutated in host. Fluoroquinolone resistance was acquired more frequently during treatment than resistance to any other anti-TB drug.ConclusionsWe show that frequently mutated genes in MTBC reveal expected and newly discovered in host adaptations, predominantly associated with DR but also with pathogenesis. The higher resistance acquisition rate observed for fluoroquinolones may have important clinical relevance.