GB virus type C infection modulates T-cell activation independently of HIV-1 viral load

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Abstract

Background:

Many clinical studies have suggested a beneficial effect of GB virus type C (GBV-C) on the course of HIV-1 infection, but the mechanisms involved in such amelioration are not clear. As recent evidence has implicated cellular activation in HIV-1 pathogenesis, we investigated the effect of GBV-C viremia on T-cell activation in early HIV-1 infection.

Methods:

Forty-eight recently infected HIV-1 patients (23 GBV-C viremic) were evaluated for T-cell counts, expanded immunophenotyping GBV-C RNA detection, and HIV-1 viral load. Nonparametric univariate and multivariate analyses were carried out to identify variables associated with cellular activation, including GBV-C status, HIV-1 viral load, T lymphocyte counts, and CD38 and chemokine (C–C motif) receptor 5 (CCR5) surface expression.

Finding:

We not only confirmed the positive correlation between HIV-1 viral load and the percentage of T cells positive for CD38+CD8+ but also observed that GBV-C viremic patients had a lower percentage of T cells positive for CD38+CD4+, CD38+CD8+, CCR5+CD4+, and CCR5+CD8+ compared with HIV-1-infected patients who were not GBV-C viremic. In regression models, GBV-C RNA+ status was associated with a reduction in the CD38 on CD4+ or CD8+ T cells and CCR5+ on CD8+ T cells, independent of the HIV-1 viral load or CD4+ and CD8+ T-cell counts. These results were also supported by the lower expression of CD69 and CD25 in GBV-C viremic patients.

Interpretation:

The association between GBV-C replication and lower T-cell activation may be a key mechanism involved in the protection conferred by this virus against HIV-1 disease progression to immunodeficiency in HIV-1-infected patients.

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