Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/31949
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dc.contributor.authorMaidana-Giret, Maria Teresa [UNIFESP]
dc.contributor.authorSilva, Tania M. [UNIFESP]
dc.contributor.authorSauer, Mariana M. [UNIFESP]
dc.contributor.authorTomiyama, Helena [UNIFESP]
dc.contributor.authorLevi, Jose Eduardo
dc.contributor.authorBassichetto, Katia Cristina
dc.contributor.authorNishiya, Anna
dc.contributor.authorDiaz, Ricardo S. [UNIFESP]
dc.contributor.authorSabino, Ester Cerdeira [UNIFESP]
dc.contributor.authorPalacios, Ricardo [UNIFESP]
dc.contributor.authorKallas, Esper Georges [UNIFESP]
dc.date.accessioned2016-01-24T13:58:55Z-
dc.date.available2016-01-24T13:58:55Z-
dc.date.issued2009-11-13
dc.identifierhttp://dx.doi.org/10.1097/QAD.0b013e32832d7a11
dc.identifier.citationAids. Philadelphia: Lippincott Williams & Wilkins, v. 23, n. 17, p. 2277-2287, 2009.
dc.identifier.issn0269-9370
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/31949-
dc.description.abstractBackground: 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 & Wilkinsen
dc.description.sponsorshipBrazilian Program for STD and AIDS, Ministry of Health
dc.description.sponsorshipSão Paulo City Health Department
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.format.extent2277-2287
dc.language.isoeng
dc.publisherLippincott Williams & Wilkins
dc.relation.ispartofAids
dc.rightsAcesso aberto
dc.subjectactivationen
dc.subjectCD38en
dc.subjectcoinfectionen
dc.subjectGB virus type Cen
dc.subjectHIV-1en
dc.subjectT lymphocyteen
dc.titleGB virus type C infection modulates T-cell activation independently of HIV-1 viral loaden
dc.typeArtigo
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionPubl Hlth Dept São Paulo
dc.contributor.institutionFundacao Prosangue
dc.description.affiliationUniv São Paulo, Lab Invest Med 60, Div Clin Immunol & Allergy, BR-01246903 São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Div Infect Dis, São Paulo, Brazil
dc.description.affiliationUniv São Paulo, Inst Trop Med, BR-01246903 São Paulo, Brazil
dc.description.affiliationPubl Hlth Dept São Paulo, São Paulo, Brazil
dc.description.affiliationFundacao Prosangue, Hemoctr, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Div Infect Dis, São Paulo, Brazil
dc.description.sponsorshipIDBrazilian Program for STD and AIDS, Ministry of Health: 914/BRA/3014-UNESCO/Kallas
dc.description.sponsorshipIDSão Paulo City Health Department: 2004-0.168.922-7/Kallas
dc.description.sponsorshipIDFAPESP: 04/15856-9/Diaz
dc.description.sponsorshipIDFAPESP: 05/01072-9/Levi)
dc.identifier.doi10.1097/QAD.0b013e32832d7a11
dc.description.sourceWeb of Science
dc.identifier.wosWOS:000271589700005
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