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Título

A metagenome-wide association study of HIV disease progression in HIV controllers

AutorReal, Luis Miguel CSIC ORCID; Sáez, María Eugenia; Corma-Gómez, Anaïs; González-Pérez, Antonio; Thorball, Christian; Ruiz, Rocío; Jiménez-León, María Reyes CSIC; González-Serna, Alejandro; Gasca-Capote, Carmen; Bravo, María José; Royo, José Luis CSIC ORCID; Pérez-Gómez, Alberto CSIC ORCID; Camacho-Sojo, María Inés; Gallego, Isabel CSIC ORCID; Vitallé, Joana CSIC ORCID; Bachiller, Sara CSIC ORCID; Gutiérrez Valencia, Alicia CSIC ORCID; Vidal, Francisco; Fellay, Jacques; Lichterfeld, Mathias; Ruiz-Mateos, Ezequiel CSIC ORCID; Swiss HIV Cohort Study
Palabras claveHealth sciences
Medicine
Natural sciences
Biological sciences
Immunology
Fecha de publicación21-jul-2023
EditorCell Press
CitacióniScience 26(7): 107214 (2023)
Resumen[Summary] Some HIV controllers experience immunologic progression with CD4+ T cell decline. We aimed to identify genetic factors associated with CD4+ T cell lost in HIV controllers. A total of 561 HIV controllers were included, 442 and 119 from the International HIV controllers Study Cohort and the Swiss HIV Cohort Study, respectively. No SNP or gene was associated with the long-term non-progressor HIV spontaneous control phenotype in the individual GWAS or in the meta-analysis. However, SNPs previously associated with natural HIV control linked to HLA-B (rs2395029 [p = 0.005; OR = 1.70], rs59440261 [p = 0.003; OR = 1.78]), MICA (rs112243036 [p = 0.011; OR = 1.45]), and PSORS1C1 loci (rs3815087 [p = 0.017; OR = 1.39]) showed nominal association with this phenotype. Genetic factors associated with the long-term HIV controllers without risk of immunologic progression are those previously related to the overall HIV controller phenotype.
Descripción© 2023 The Authors. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
Versión del editorhttps://doi.org/10.1016/j.isci.2023.107214
URIhttp://hdl.handle.net/10261/349330
DOI10.1016/j.isci.2023.107214
E-ISSN2589-0042
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