Evidence map›Paper›PMID 21160409›Full record

ArticleAIDS (London, England)2011

Common human genetic variants and HIV-1 susceptibility: a genome-wide survey in a homogeneous African population.

Slavé Petrovski, Jacques Fellay, Kevin V Shianna, Nicole Carpenetti, Johnstone Kumwenda, Gift Kamanga, Deborah D Kamwendo, Norman L Letvin, Andrew J McMichael, Barton F Haynes and 3 more

Open access · greenAbstract read
In one paragraph

Article in AIDS (London, England), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 4 pooled it
3.4field-weighted citation impact, top 7% 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

51 citing papers in PubMed, 4 syntheses or guidelines pooled it, 85 citations in OpenAlex.

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  7. HIV-1 and human genetic variation.Nature reviews. Genetics · 2021
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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

13 authors at 6 institutions in 4 countries.

Slavé PetrovskiCenter for Human Genome Variation, School of Medicine, Duke University, Durham, North Carolina 27708, USA. slave.petrovski@duke.edu
Jacques Fellay
Kevin V Shianna
Nicole Carpenetti
Johnstone Kumwenda
Gift Kamanga
Deborah D Kamwendo
Norman L Letvin
Andrew J McMichael
Barton F Haynes
Myron S Cohen
David B Goldstein
Center for HIV/AIDS Vaccine Immunology
Duke University · USUniversity of Malawi · MWBeth Israel Deaconess Medical Center · USGTx (United States) · USJohn Radcliffe Hospital · GBUniversity of North Carolina at Chapel Hill · US

Funding

Viral Sequencing CoreU19AI067854 · NIAID · DUKE UNIVERSITY · PI BHARDWAJ, NINA · 2006 to 2011
$290.5M
Viral and Host Determinants of HIV-1 TransmissionU01AI067854 · NIAID · DUKE UNIVERSITY · PI HAYNES, BARTON F · 2005 to 2005
$14.9M
Medical Research Council MC_U137884177NIAID NIH HHS AI067854NIAID NIH HHS U01 AI067854NIAID NIH HHS U19 AI067854
6 · The paper itself

Abstract

objectiveTo date, CCR5 variants remain the only human genetic factors to be confirmed to impact HIV-1 acquisition. However, protective CCR5 variants are largely absent in African populations, in which sporadic resistance to HIV-1 infection is still unexplained. We investigated whether common genetic variants associate with HIV-1 susceptibility in Africans.

methodsWe performed a genome-wide association study (GWAS) in a population of 1532 individuals from Malawi, a country with high prevalence of HIV-1 infection. Using single-nucleotide polymorphisms (SNPs) present on the genome-wide chip, we also investigated previously reported associations with HIV-1 susceptibility or acquisition. Recruitment was coordinated by the Center for HIV/AIDS Vaccine Immunology at two sexually transmitted infection clinics. HIV status was determined by HIV rapid tests and nucleic acid testing.

resultsAfter quality control, the population consisted of 848 high-risk seronegative and 531 HIV-1 seropositive individuals. Logistic regression testing in an additive genetic model was performed for SNPs that passed quality control. No single SNP yielded a significant P value after correction for multiple testing. The study was sufficiently powered to detect markers with genotype relative risk 2.0 or more and minor allele frequencies 12% or more.

conclusionThis is the first GWAS of host determinants of HIV-1 susceptibility, performed in an African population. The absence of any significant association can have many possible explanations: rarer genetic variants or common variants with weaker effect could be responsible for the resistance phenotype; alternatively, resistance to HIV-1 infection might be due to nongenetic parameters or to complex interactions between genes, immunity and environment.

Indexed as

Genetic Predisposition to DiseaseHIV-1AdolescentAdultBlack PeopleFemaleGenome-Wide Association StudyHIV InfectionsHumansMalawiMaleMiddle AgedPhenotypeReceptors, CCR5Young AdultReceptors, CCR5

Identifiers

PMID21160409
PMCPMC3150594
OpenAlexW1996494492

What OpenQuestion holds

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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.