{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["McLaren PJ"],"funding":["NIDA NIH HHS","Howard Hughes Medical Institute","NIAID NIH HHS"],"pagination":["14658-63"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4664299"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["112(47)"],"pubmed_abstract":["Previous genome-wide association studies (GWAS) of HIV-1-infected populations have been underpowered to detect common variants with moderate impact on disease outcome and have not assessed the phenotypic variance explained by genome-wide additive effects. By combining the majority of available genome-wide genotyping data in HIV-infected populations, we tested for association between ∼8 million variants and viral load (HIV RNA copies per milliliter of plasma) in 6,315 individuals of European ancestry. The strongest signal of association was observed in the HLA class I region that was fully explained by independent effects mapping to five variable amino acid positions in the peptide binding grooves of the HLA-B and HLA-A proteins. We observed a second genome-wide significant association sign"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["Polymorphisms of large effect explain the majority of the host genetic contribution to variation of HIV-1 virus load."],"pmcid":["PMC4664299"],"funding_grant_id":["P01 AI057005","U01 DA036297","K24 AI118591","R01 DA012568","R01 AI077505"],"pubmed_authors":["Walker BD","Wolinsky SM","van Manen D","Goldstein DB","McLaren PJ","Herbeck JT","Zagury JF","Raychaudhuri S","Cossarizza A","Theodorou I","Poli G","Schuitemaker H","Fellay J","Mullins JI","de Bakker PI","Haas DW","De Luca A","Martinez-Picado J","Goedert JJ","Bartha I","Winkler CA","Shea PR","Carrington MN","Coulonges C","Lenz TL","Meyer L","Obel N","Miro JM","Lambotte O","Deutsch AJ","Kirk GD","Bashirova A","Mallal S","Telenti A","Luo M","Sandhu MS","Weintrob AC","Buchbinder S","Dalmau J","Johnson EO","Gurdasani D"],"additional_accession":[]},"is_claimable":false,"name":"Polymorphisms of large effect explain the majority of the host genetic contribution to variation of HIV-1 virus load.","description":"Previous genome-wide association studies (GWAS) of HIV-1-infected populations have been underpowered to detect common variants with moderate impact on disease outcome and have not assessed the phenotypic variance explained by genome-wide additive effects. By combining the majority of available genome-wide genotyping data in HIV-infected populations, we tested for association between ∼8 million variants and viral load (HIV RNA copies per milliliter of plasma) in 6,315 individuals of European ancestry. The strongest signal of association was observed in the HLA class I region that was fully explained by independent effects mapping to five variable amino acid positions in the peptide binding grooves of the HLA-B and HLA-A proteins. We observed a second genome-wide significant association sign","dates":{"release":"2015-01-01T00:00:00Z","publication":"2015 Nov","modification":"2026-05-05T07:53:40.331Z","creation":"2019-03-27T02:02:58Z"},"accession":"S-EPMC4664299","cross_references":{"pubmed":["26553974"],"doi":["10.1073/pnas.1514867112"]}}