Evidence map›Paper›PMID 24171102›Full record

ArticleeLife2013

A genome-to-genome analysis of associations between human genetic variation, HIV-1 sequence diversity, and viral control.

István Bartha, Jonathan M Carlson, Chanson J Brumme, Paul J McLaren, Zabrina L Brumme, Mina John, David W Haas, Javier Martinez-Picado, Judith Dalmau, Cecilio López-Galíndez and 19 more

Abstract read
In one paragraph

Article in eLife, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed
–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

91 citing papers in PubMed.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. BeyondFrontiers in genetics · 2026
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Prediction of resistance, virulence, and host-by-pathogen interactions using dual-genome prediction models.TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik · 2024
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

31 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

29 authors.

István BarthaSchool of Life Sciences , École Polytechnique Fédérale de Lausanne , Lausanne , Switzerland ; Institute of Microbiology , University Hospital and University of Lausanne , Lausanne , Switzerland ; Research Group of Theoretical Biology and Evolutionary Ecology , Eötvös Loránd University and the Hungarian Academy of Sciences , Budapest , Hungary ; Swiss Institute of Bioinformatics , Lausanne , Switzerland.
Jonathan M Carlson
Chanson J Brumme
Paul J McLaren
Zabrina L Brumme
Mina John
David W Haas
Javier Martinez-Picado
Judith Dalmau
Cecilio López-Galíndez
Concepción Casado
Andri Rauch
Huldrych F Günthard
Enos Bernasconi
Pietro Vernazza
Thomas Klimkait
Sabine Yerly
Stephen J O'Brien
Jennifer Listgarten
Nico Pfeifer
Christoph Lippert
Nicolo Fusi
Zoltán Kutalik
Todd M Allen
Viktor Müller
P Richard Harrigan
David Heckerman
Amalio Telenti
Jacques Fellay

Funding

Recognition of HIV-1 by Innate Immunity Receptors during Primary InfectionP01AI074415 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI ALLEN, TODD M · 2008 to 2013
$17.3M
NIAID NIH HHS P01 AI074415
6 · The paper itself

Abstract

HIV-1 sequence diversity is affected by selection pressures arising from host genomic factors. Using paired human and viral data from 1071 individuals, we ran >3000 genome-wide scans, testing for associations between host DNA polymorphisms, HIV-1 sequence variation and plasma viral load (VL), while considering human and viral population structure. We observed significant human SNP associations to a total of 48 HIV-1 amino acid variants (p<2.4 × 10(-12)). All associated SNPs mapped to the HLA class I region. Clinical relevance of host and pathogen variation was assessed using VL results. We identified two critical advantages to the use of viral variation for identifying host factors: (1) association signals are much stronger for HIV-1 sequence variants than VL, reflecting the 'intermediate phenotype' nature of viral variation; (2) association testing can be run without any clinical data. The proposed genome-to-genome approach highlights sites of genomic conflict and is a strategy generally applicable to studies of host-pathogen interaction. DOI:http://dx.doi.org/10.7554/eLife.01123.001.

Indexed as

Genome, HumanGenome, ViralPolymorphism, Single NucleotideAllelesGenome-Wide Association StudyHistocompatibility Antigens Class IHIV-1HIV InfectionsHost-Pathogen InteractionsHumansViral LoadHistocompatibility Antigens Class IHIVHumanhuman genomicsviral mutations

Identifiers

PMID24171102
PMCPMC3807812

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.