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

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

Author Maidana-Giret, Maria Teresa Autor UNIFESP Google Scholar
Silva, Tania M. Autor UNIFESP Google Scholar
Sauer, Mariana M. Autor UNIFESP Google Scholar
Tomiyama, Helena Autor UNIFESP Google Scholar
Levi, Jose Eduardo Google Scholar
Bassichetto, Katia Cristina Google Scholar
Nishiya, Anna Google Scholar
Diaz, Ricardo S. Autor UNIFESP Google Scholar
Sabino, Ester Cerdeira Autor UNIFESP Google Scholar
Palacios, Ricardo Autor UNIFESP Google Scholar
Kallas, Esper Georges Autor UNIFESP Google Scholar
Institution Universidade de São Paulo (USP)
Universidade Federal de São Paulo (UNIFESP)
Publ Hlth Dept São Paulo
Fundacao Prosangue
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
Keywords activation
CD38
coinfection
GB virus type C
HIV-1
T lymphocyte
Language English
Sponsor Brazilian Program for STD and AIDS, Ministry of Health
São Paulo City Health Department
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
Grant number Brazilian Program for STD and AIDS, Ministry of Health: 914/BRA/3014-UNESCO/Kallas
São Paulo City Health Department: 2004-0.168.922-7/Kallas
FAPESP: 04/15856-9/Diaz
FAPESP: 05/01072-9/Levi)
Date 2009-11-13
Published in Aids. Philadelphia: Lippincott Williams & Wilkins, v. 23, n. 17, p. 2277-2287, 2009.
ISSN 0269-9370 (Sherpa/Romeo, impact factor)
Publisher Lippincott Williams & Wilkins
Extent 2277-2287
Origin http://dx.doi.org/10.1097/QAD.0b013e32832d7a11
Access rights Open access Open Access
Type Article
Web of Science ID WOS:000271589700005
URI http://repositorio.unifesp.br/handle/11600/31949

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