{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Armani-Tourret M"],"funding":["INSERM","Instituto de Salud Carlos III","Agence Nationale de la Recherche","Agence Nationale de Recherches sur le Sida et les Hépatites Virales","Université Toulouse III - Paul Sabatier","Institut Pasteur","Sidaction"],"pagination":["e1009526"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8084328"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["17(4)"],"pubmed_abstract":["HIV-1 infects CD4 T lymphocytes (CD4TL) through binding the chemokine receptors CCR5 or CXCR4. CXCR4-using viruses are considered more pathogenic, linked to accelerated depletion of CD4TL and progression to AIDS. However, counterexamples to this paradigm are common, suggesting heterogeneity in the virulence of CXCR4-using viruses. Here, we investigated the role of the CXCR4 chemokine CXCL12 as a driving force behind virus virulence. In vitro, CXCL12 prevents HIV-1 from binding CXCR4 and entering CD4TL, but its role in HIV-1 transmission and propagation remains speculative. Through analysis of thirty envelope glycoproteins (Envs) from patients at different stages of infection, mostly treatment-naïve, we first interrogated whether sensitivity of viruses to inhibition by CXCL12 varies over ti"],"journal":["PLoS pathogens"],"pubmed_title":["Mechanisms of HIV-1 evasion to the antiviral activity of chemokine CXCL12 indicate potential links with pathogenesis."],"pmcid":["PMC8084328"],"funding_grant_id":["AAP-2013-2 and ECTZ63419","RD16CIII/0002/0001","ANR-10-LABX-69-01","PI19CIIII/0004"],"pubmed_authors":["Staropoli I","Perez-Olmeda M","Assoumou L","Levy Y","Benureau Y","Armani-Tourret M","Gasser R","Alcami J","Mouquet H","Garcia-Perez J","Lagane B","Zhou Z","Lorin V","Puissant-Lubrano B","Arenzana-Seisdedos F","Cantaloube-Ferrieu V","Martin-Blondel G","Izopet J","Colin P","Delaugerre C","Lelievre JD"],"additional_accession":[]},"is_claimable":false,"name":"Mechanisms of HIV-1 evasion to the antiviral activity of chemokine CXCL12 indicate potential links with pathogenesis.","description":"HIV-1 infects CD4 T lymphocytes (CD4TL) through binding the chemokine receptors CCR5 or CXCR4. CXCR4-using viruses are considered more pathogenic, linked to accelerated depletion of CD4TL and progression to AIDS. However, counterexamples to this paradigm are common, suggesting heterogeneity in the virulence of CXCR4-using viruses. Here, we investigated the role of the CXCR4 chemokine CXCL12 as a driving force behind virus virulence. In vitro, CXCL12 prevents HIV-1 from binding CXCR4 and entering CD4TL, but its role in HIV-1 transmission and propagation remains speculative. Through analysis of thirty envelope glycoproteins (Envs) from patients at different stages of infection, mostly treatment-naïve, we first interrogated whether sensitivity of viruses to inhibition by CXCL12 varies over ti","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Apr","modification":"2026-05-08T10:55:30.153Z","creation":"2025-02-19T00:19:01.271Z"},"accession":"S-EPMC8084328","cross_references":{"pubmed":["33872329"],"doi":["10.1371/journal.ppat.1009526"]}}