Evidence map›Paper›PMID 22312052›Full record

ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2012

Host-pathogen coevolution in human tuberculosis.

Sebastien Gagneux

Open access · bronzeAbstract readHistorical ArticleReview
In one paragraph

Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 194 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
194citing papers in PubMed, 2 pooled it
17.2field-weighted citation impact, top 1% 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

194 citing papers in PubMed, 2 syntheses or guidelines pooled it, 429 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Polyketide synthase 12 is anbioRxiv : the preprint server for biology · 2026
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  13. Population structure and spatial distribution ofFrontiers in microbiology · 2026
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  18. Experimental dissection of tuberculosis protective immunity: a human perspective.Frontiers in cellular and infection microbiology · 2025
    Review
  19. Article
  20. Article

134 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Sebastien GagneuxDepartment of Medical Parasitology and Infection Biology, Swiss Tropical and Public Health Institute and University of Basel, Basel, Switzerland. sebastien.gagneux@unibas.ch
Swiss Tropical and Public Health Institute · CH

Funding

POPULATION-BASED MOLECULAR EPIDEMIOLOGY OF TUBERCULOSISR01AI034238 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HOPEWELL, PHILIP C · 1993 to 2010
$9.3M
Mycobacterium tuberculosis antigen diversityR01AI090928 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ERNST, JOEL D., GAGNEUX, SEBASTIEN · 2010 to 2014
$3.2M
Medical Research Council MRC_U117588500NIAID NIH HHS AI034238NIAID NIH HHS AI090928NIAID NIH HHS R01 AI034238NIAID NIH HHS R01 AI090928
6 · The paper itself

Abstract

Tuberculosis (TB) is a disease of antiquity. Yet TB today still causes more adult deaths than any other single infectious disease. Recent studies show that contrary to the common view postulating an animal origin for TB, Mycobacterium tuberculosis complex (MTBC), the causative agent of TB, emerged as a human pathogen in Africa and colonized the world accompanying the Out-of-Africa migrations of modern humans. More recently, evolutionarily 'modern' lineages of MTBC expanded as a consequence of the global human population increase, and spread throughout the world following waves of exploration, trade and conquest. While epidemiological data suggest that the different phylogenetic lineages of MTBC might have adapted to different human populations, overall, the phylogenetically 'modern' MTBC lineages are more successful in terms of their geographical spread compared with the 'ancient' lineages. Interestingly, the global success of 'modern' MTBC correlates with a hypo-inflammatory phenotype in macrophages, possibly reflecting higher virulence, and a shorter latency in humans. Finally, various human genetic variants have been associated with different MTBC lineages, suggesting an interaction between human genetic diversity and MTBC variation. In summary, the biology and the epidemiology of human TB have been shaped by the long-standing association between MTBC and its human host.

Indexed as

Evolution, MolecularGenetic VariationPhylogenyDemographyEmigration and ImmigrationHistory, AncientHost-Pathogen InteractionsHumansMycobacterium tuberculosisPhylogeographyTuberculosisVirulence

Identifiers

PMID22312052
PMCPMC3267123
OpenAlexW2145407927

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.