Evidence map›Paper›PMID 40019877›Full record

ReviewPLoS pathogens2025

Understanding Mycobacterium tuberculosis through its genomic diversity and evolution.

Mollie I Sweeney, Carson E Carranza, David M Tobin

Abstract readReview
In one paragraph

Review in PLoS pathogens, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
–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

12 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Protein Architecture and Composition in Mycobacterium tuberculosis.Advances in experimental medicine and biology · 2026
    Review
  10. Review
  11. Review
  12. Frontiers in tuberculosis · 2025
    Review
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

3 authors.

Mollie I SweeneyDepartment of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, North Carolina, USA.
Carson E CarranzaDepartment of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, North Carolina, USA.
David M TobinDepartment of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, North Carolina, USA.ORCID 0000-0003-3465-5518

Funding

Macrophage Reprogramming During Granuloma Formation in the ZebrafishR01AI130236 · NIAID · DUKE UNIVERSITY · PI David M. Tobin · 2017 to 2026
$4.5M
Genetic dissection of angiogenesis in the tuberculous granulomaR01AI125517 · NIAID · DUKE UNIVERSITY · PI David M. Tobin · 2017 to 2026
$4.4M
Linking Human TB Genetic Susceptibility Loci to Granuloma BiologyR01AI166304 · NIAID · DUKE UNIVERSITY · PI David M. Tobin · 2022 to 2026
$3.4M
The Genetic Basis of Bone Disease in Mycobacterial InfectionR01AI127715 · NIAID · DUKE UNIVERSITY · PI Clare Margaret Smith, David M. Tobin · 2017 to 2026
$3.3M
NIAID NIH HHS R01 AI125517NIAID NIH HHS R01 AI127715NIAID NIH HHS R01 AI130236NIAID NIH HHS R01 AI166304
6 · The paper itself

Abstract

Pathogen evolution and genomic diversity are shaped by specific host immune pressures and therapeutic interventions. Analysis of the extant genomes of circulating strains of Mycobacterium tuberculosis, a leading cause of infectious mortality that has co-evolved with humans for thousands of years, can provide new insights into host-pathogen interactions that underlie specific aspects of pathogenesis and onward transmission. With the explosion in the number of fully sequenced M. tuberculosis strains that are now paired with detailed clinical data, there are new opportunities to understand the evolutionary basis for and consequences of M. tuberculosis strain diversity. This review examines mechanistic findings that have emerged from pairing whole genome sequencing data and evolutionary analysis with functional dissection of specific bacterial variants. These include improved understanding of secreted effectors that modulate the properties and migratory behavior of infected macrophages as well as bacterial genetic alterations important for survival within hypoxic microenvironments. Genomic, evolutionary, and functional analyses across diverse M. tuberculosis strains will identify prominent bacterial adaptations to their human hosts and shape our understanding of TB disease biology and the host immune response.

Indexed as

Evolution, MolecularGenetic VariationGenome, BacterialHost-Pathogen InteractionsMycobacterium tuberculosisTuberculosisAnimalsGenomicsHumans

Identifiers

PMID40019877
PMCPMC11870338

What OpenQuestion holds

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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.