Evidence map›Paper›PMID 22312051›Full record

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

Evolution, revolution and heresy in the genetics of infectious disease susceptibility.

Adrian V S Hill

Registry-linked trialOpen access · bronzeAbstract readReview
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. It is linked to trial NCT02832843 (Elucidation of Genetic Susceptibility of Patients With Nontuberculous Mycobacterial Lung Disease Using Genome-Wide Association Study), which is not on this map. Cited by 60 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 2 pooled it
5.3field-weighted citation impact, top 3% 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.

NCT02832843 completednot on this mapstarted 2016, after this paper: background citation

Elucidation of Genetic Susceptibility of Patients With Nontuberculous Mycobacterial Lung Disease Using Genome-Wide Association Study

TypeobservationalSponsorSeoul National University HospitalRan2016 to 2019Enrolled2,808ConditionsMycobacterium Infections, Nontuberculous
3 · Its place in the literature

Who cites it

60 citing papers in PubMed, 2 syntheses or guidelines pooled it, 131 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Host- and pathogen-related determinants of pulmonaryEuropean respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  5. Article
  6. Prognostic Value ofBalkan journal of medical genetics : BJMG · 2023
    Article
  7. Article
  8. Article
  9. A novel transposable element-mediated mechanism causes antiviral resistance inProceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  10. Observational
  11. Article
  12. Article
  13. Genetics of Host Protection againstInternational journal of molecular sciences · 2021
    Review
  14. Review
  15. Review
  16. An immunogenetic view of COVID-19.Genetics and molecular biology · 2021
    Article
  17. Review
  18. Article
  19. Review
  20. 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

1 author at 1 institution in 1 country.

Adrian V S HillWellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK. adrian.hill@well.ox.ac.uk
University of Oxford · GB

Funding

Medical Research CouncilWellcome Trust 090532
6 · The paper itself

Abstract

Infectious pathogens have long been recognized as potentially powerful agents impacting on the evolution of human genetic diversity. Analysis of large-scale case-control studies provides one of the most direct means of identifying human genetic variants that currently impact on susceptibility to particular infectious diseases. For over 50 years candidate gene studies have been used to identify loci for many major causes of human infectious mortality, including malaria, tuberculosis, human immunodeficiency virus/acquired immunodeficiency syndrome, bacterial pneumonia and hepatitis. But with the advent of genome-wide approaches, many new loci have been identified in diverse populations. Genome-wide linkage studies identified a few loci, but genome-wide association studies are proving more successful, and both exome and whole-genome sequencing now offer a revolutionary increase in power. Opinions differ on the extent to which the genetic component to common disease susceptibility is encoded by multiple high frequency or rare variants, and the heretical view that most infectious diseases might even be monogenic has been advocated recently. Review of findings to date suggests that the genetic architecture of infectious disease susceptibility may be importantly different from that of non-infectious diseases, and it is suggested that natural selection may be the driving force underlying this difference.

Indexed as

Evolution, MolecularGenetic VariationSelection, GeneticCommunicable DiseasesGenetic Association StudiesGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansImmunity, InnateSignal Transduction

Identifiers

PMID22312051
PMCPMC3267114
OpenAlexW2147786362

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.