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

Author(s):Show less -

Maidana-Giret, Maria Teresa ^[1] ; Silva, Tania M. ^[1] ; Sauer, Mariana M. ^[1] ; Tomiyama, Helena ^[1] ; Levi, Jose Eduardo ^[2] ; Bassichetto, Katia C. ^[3] ; Nishiya, Anna ^[4] ; Diaz, Ricardo S. ^[1] ; Sabino, Ester C. ^[4] ; Palacios, Ricardo ^[1] ; Kallas, Esper Georges ^{[1, 5]}

Affiliation

^[1] Univ Fed Sao Paulo, Div Infect Dis, Sao Paulo - Brazil

^[2] Univ Sao Paulo, Inst Trop Med, BR-01246903 Sao Paulo - Brazil

^[3] Publ Hlth Dept Sao Paulo, Sao Paulo - Brazil

^[4] Fundacao Prosangue, Hemoctr, Sao Paulo - Brazil

^[5] Univ Sao Paulo, Lab Invest Med 60, Div Clin Immunol & Allergy, BR-01246903 Sao Paulo - Brazil

• Document type: Journal article
• Source: AIDS; v. 23, n. 17, p. 2277-2287, NOV 13 2009.
• Web of Science Citations: 35

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. (C) 2009 Wolters Kluwer Health | Lippincott Williams \& Wilkins (AU)

• FAPESP's process: 04/15856-9 - Prospective analysis of the virological and immunological characteristics in individuals with recent HIV-1 infection in the cities of São Paulo and Santos
• Grantee: Ricardo Sobhie Diaz
• Support Opportunities: Research Projects - Thematic Grants
• FAPESP's process: 05/01072-9 - GB virus C/HGV and prognosis on HIV infected women
• Grantee: José Eduardo Levi
• Support Opportunities: Regular Research Grants