SynthesisPLoS pathogens2013
Association study of common genetic variants and HIV-1 acquisition in 6,300 infected cases and 7,200 controls.
Synthesis in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 2 of them syntheses that pooled 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.
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.
Who cites it
73 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Interleukin gene polymorphisms and susceptibility to HIV-1 infection: a meta-analysis.Journal of genetics · 2018Pooled it
- A genome-wide association meta-analysis of diarrhoeal disease in young children identifies FUT2 locus and provides plausible biological pathways.Human molecular genetics · 2016Pooled it
- Association Between Single-Nucleotide Polymorphisms in HLA Alleles and Human Immunodeficiency Virus Type 1 Viral Load in Demographically Diverse, Antiretroviral Therapy-Naive Participants From the Strategic Timing of AntiRetroviral Treatment Trial.The Journal of infectious diseases · 2019Trial
- Human genetic variants and age are the strongest predictors of humoral immune responses to common pathogens and vaccines.Genome medicine · 2018Trial
- Clinical and demographic factors associated with low viral load in early untreated HIV infection in the INSIGHT Strategic Timing of AntiRetroviral Treatment (START) trial.HIV medicine · 2015Trial
- Co-regulation of HIV control and cytomegalovirus pp65-specific IL-1β and TNF-α responses by genetic variants in the MHC region.PLoS pathogens · 2026Article
- Antiretroviral therapy blocks natural selection on protective and disease-susceptible HLA-B alleles in HIV-1 infection.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- BeyondFrontiers in genetics · 2026Review
- The HLA-B*57:01 Haplotype, Genetic Key Linking Innate Immunity and Longevity.Aging and disease · 2025Article
- Causal role of immunophenotypes in HIV-1 acquisition: insights from Mendelian randomization analysis.Scientific reports · 2025Article
- Immune Alterations and Viral Reservoir Atlas in SIV-Infected Chinese Rhesus Macaques.Infectious disease reports · 2025Review
- Functionally-informed fine-mapping identifies genetic variants linking increased CHD1L expression and HIV restriction in monocytes.Scientific reports · 2025Article
- Article
- Exceptional, naturally occurring HIV-1 control: Insight into a functional cure.Med (New York, N.Y.) · 2024Review
- Genetic Association Studies in Host-Pathogen Interaction Analysis.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Association of TREX1 polymorphism with disease progression in human immunodeficiency virus type-1 (HIV-1) infected patients.Virus genes · 2023Article
- Article
- Omics and systems view of innate immune pathways.Proteomics · 2023Review
- Multiancestry sex-stratified genomic associations with HIV viral load and controller status from the ICGH.JCI insight · 2023Article
- CCR5∆32 and SDF1 3'A: Gene Variants, Expression and Influence on Biological Markers for the Clinical Progression to AIDS among HIV-1 Virus Controllers in a Mixed Population of the Amazon Region of Brazil.International journal of molecular sciences · 2023Article
13 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
46 authors.
Funding
Abstract
Multiple genome-wide association studies (GWAS) have been performed in HIV-1 infected individuals, identifying common genetic influences on viral control and disease course. Similarly, common genetic correlates of acquisition of HIV-1 after exposure have been interrogated using GWAS, although in generally small samples. Under the auspices of the International Collaboration for the Genomics of HIV, we have combined the genome-wide single nucleotide polymorphism (SNP) data collected by 25 cohorts, studies, or institutions on HIV-1 infected individuals and compared them to carefully matched population-level data sets (a list of all collaborators appears in Note S1 in Text S1). After imputation using the 1,000 Genomes Project reference panel, we tested approximately 8 million common DNA variants (SNPs and indels) for association with HIV-1 acquisition in 6,334 infected patients and 7,247 population samples of European ancestry. Initial association testing identified the SNP rs4418214, the C allele of which is known to tag the HLA-B*57:01 and B*27:05 alleles, as genome-wide significant (p = 3.6 × 10⁻¹¹). However, restricting analysis to individuals with a known date of seroconversion suggested that this association was due to the frailty bias in studies of lethal diseases. Further analyses including testing recessive genetic models, testing for bulk effects of non-genome-wide significant variants, stratifying by sexual or parenteral transmission risk and testing previously reported associations showed no evidence for genetic influence on HIV-1 acquisition (with the exception of CCR5Δ32 homozygosity). Thus, these data suggest that genetic influences on HIV acquisition are either rare or have smaller effects than can be detected by this sample size.
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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.