SynthesisThe Journal of infectious diseases2026
In Host Mutational Adaptation of Mycobacterium Tuberculosis Complex Strains During Tuberculosis Infection.
Synthesis in The Journal of infectious diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Variation in multiple classes of simple sequence repeats can alter drug susceptibility inbioRxiv : the preprint server for biology · 2026Article
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5 authors.
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Abstract
backgroundTuberculosis (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.
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