dc.creatorAguilar Jiménez, Wbeimar
dc.creatorVillegas Ospina, Simón
dc.creatorGonzález Díaz, Sandra Milena
dc.creatorZapata Builes, Wildeman
dc.creatorSaulle, Irma
dc.creatorGarziano, Micaela
dc.creatorBiasin, Mara
dc.creatorClerici, Mario
dc.creatorRugeles López, María Teresa
dc.date2022-07-25T20:29:55Z
dc.date2022-07-25T20:29:55Z
dc.date2016
dc.date.accessioned2023-08-28T19:42:04Z
dc.date.available2023-08-28T19:42:04Z
dc.identifierAguilar-Jiménez W, Villegas-Ospina S, González S, Zapata W, Saulle I, Garziano M, Biasin M, Clerici M, Rugeles MT. Precursor Forms of Vitamin D Reduce HIV-1 Infection In Vitro. J Acquir Immune Defic Syndr. 2016 Dec 15;73(5):497-506. doi: 10.1097/QAI.0000000000001150.
dc.identifier1525-4135
dc.identifierhttps://hdl.handle.net/10495/29861
dc.identifier10.1097/QAI.0000000000001150
dc.identifier1944-7884
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8466779
dc.descriptionABSTRACT: Background: Although the anti-HIV-1 effects of vitamin D (VitD) have been reported, mechanisms behind such protection remain largely unexplored. Methods: The effects of two precursor forms (cholecalciferol/calciol at 0.01, 1 and 100 nM and calcidiol at 100 and 250 nM) on HIV-1 infection, immune activation, and gene expression were analyzed in vitro in cells of Colombian and Italian healthy donors. We quantified levels of released p24 by enzyme-linked immunosorbent assay, of intracellular p24 and cell-surface expression of CD38 and HLA-DR by flow cytometry, and mRNA expression of antiviral and immunoregulatory genes by real-time reverse transcription-polymerase chain reaction. Results: Cholecalciferol decreased the frequency of HIV-1-infected p24CD4 T cells and levels of p24 in supernatants in a dose-dependent manner. Moreover, the CD4CD38HLA-DR and CD4CD38HLA-DR subpopulations were more susceptible to infection but displayed the greatest cholecalciferol-induced decreases in infection rate by an X4-tropic strain. Likewise, cholecalciferol at its highest concentration decreased the frequency of CD38HLA-DR but not of CD38HLA-DR T-cell subsets. Analyzing the effects of calcidiol, the main VitD source for immune cells and an R5-tropic strain as the most frequently transmitted virus, a reduction in HIV-1 productive infection was also observed. In addition, an increase in mRNA expression of APOBEC3G and PI3 and a reduction of TRIM22 and CCR5 expression, this latter positively correlated with p24 levels, was noted. Conclusions: VitD reduces HIV-1 infection in T cells possibly by inducing antiviral gene expression, reducing the viral co-receptor CCR5 and, at least at the highest cholecalciferol concentration, by promoting an HIV-1-restrictive CD38HLA-DR immunophenotype.
dc.descriptionCOL0012444
dc.format10
dc.formatapplication/pdf
dc.formatapplication/pdf
dc.languageeng
dc.publisherWilliams & Wilkins
dc.publisherInmunovirología
dc.publisherHagerstown, Estados Unidos
dc.relationJ. Acquir. Immune Defic. Syndr.
dc.rightsinfo:eu-repo/semantics/openAccess
dc.rightshttp://creativecommons.org/licenses/by-nc-nd/2.5/co/
dc.rightshttp://purl.org/coar/access_right/c_abf2
dc.rightshttps://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subjectVIH-1
dc.subjectHIV-1
dc.subjectADP-Ribosil Ciclasa 1
dc.subjectADP-ribosyl Cyclase 1
dc.subjectVitamina D
dc.subjectVitamin D
dc.subjectLinfocitos T
dc.subjectT-Lymphocytes
dc.subjectAntígenos HLA-DR
dc.subjectHLA-DR Antigens
dc.subjectCD38
dc.titlePrecursor forms of Vitamin D reduce HIV-1 infection in vitro
dc.typeinfo:eu-repo/semantics/article
dc.typeinfo:eu-repo/semantics/publishedVersion
dc.typehttp://purl.org/coar/resource_type/c_2df8fbb1
dc.typehttps://purl.org/redcol/resource_type/ART
dc.typeArtículo de investigación


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