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Precursor Forms of Vitamin D Reduce HIV-1 Infection In Vitro.

Precursor Forms of Vitamin D Reduce HIV-1 Infection In Vitro.
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Aguilar-Jimenez W, Villegas-Ospina S, Gonzalez S, Zapata W, Saulle I, Garziano M, Biasin M, Clerici M, Rugeles MT,


Aguilar-Jimenez W, Villegas-Ospina S, Gonzalez S, Zapata W, Saulle I, Garziano M, Biasin M, Clerici M, Rugeles MT, (click to view)

Aguilar-Jimenez W, Villegas-Ospina S, Gonzalez S, Zapata W, Saulle I, Garziano M, Biasin M, Clerici M, Rugeles MT,

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Journal of acquired immune deficiency syndromes (1999) 73(5) 497-506

Abstract
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.

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