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

Detalhes bibliográficos
Autor(a) principal: Maidana-Giret, Maria Teresa [UNIFESP]
Data de Publicação: 2009
Outros Autores: Silva, Tania M. [UNIFESP], Sauer, Mariana M. [UNIFESP], Tomiyama, Helena [UNIFESP], Levi, Jose Eduardo, Bassichetto, Katia Cristina, Nishiya, Anna, Diaz, Ricardo S. [UNIFESP], Sabino, Ester Cerdeira [UNIFESP], Palacios, Ricardo [UNIFESP], Kallas, Esper Georges [UNIFESP]
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNIFESP
Texto Completo: http://dx.doi.org/10.1097/QAD.0b013e32832d7a11
http://repositorio.unifesp.br/handle/11600/31949
Resumo: 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
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spelling GB virus type C infection modulates T-cell activation independently of HIV-1 viral loadactivationCD38coinfectionGB virus type CHIV-1T lymphocyteBackground: 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 & WilkinsUniv São Paulo, Lab Invest Med 60, Div Clin Immunol & Allergy, BR-01246903 São Paulo, BrazilUniversidade Federal de São Paulo, Div Infect Dis, São Paulo, BrazilUniv São Paulo, Inst Trop Med, BR-01246903 São Paulo, BrazilPubl Hlth Dept São Paulo, São Paulo, BrazilFundacao Prosangue, Hemoctr, São Paulo, BrazilUniversidade Federal de São Paulo, Div Infect Dis, São Paulo, BrazilWeb of ScienceBrazilian Program for STD and AIDS, Ministry of HealthSão Paulo City Health DepartmentFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Brazilian Program for STD and AIDS, Ministry of Health: 914/BRA/3014-UNESCO/KallasSão Paulo City Health Department: 2004-0.168.922-7/KallasFAPESP: 04/15856-9/DiazFAPESP: 05/01072-9/Levi)Lippincott Williams & WilkinsUniversidade de São Paulo (USP)Universidade Federal de São Paulo (UNIFESP)Publ Hlth Dept São PauloFundacao ProsangueMaidana-Giret, Maria Teresa [UNIFESP]Silva, Tania M. [UNIFESP]Sauer, Mariana M. [UNIFESP]Tomiyama, Helena [UNIFESP]Levi, Jose EduardoBassichetto, Katia CristinaNishiya, AnnaDiaz, Ricardo S. [UNIFESP]Sabino, Ester Cerdeira [UNIFESP]Palacios, Ricardo [UNIFESP]Kallas, Esper Georges [UNIFESP]2016-01-24T13:58:55Z2016-01-24T13:58:55Z2009-11-13info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersion2277-2287http://dx.doi.org/10.1097/QAD.0b013e32832d7a11Aids. Philadelphia: Lippincott Williams & Wilkins, v. 23, n. 17, p. 2277-2287, 2009.10.1097/QAD.0b013e32832d7a110269-9370http://repositorio.unifesp.br/handle/11600/31949WOS:000271589700005engAidsinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP2024-10-10T10:58:58Zoai:repositorio.unifesp.br/:11600/31949Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestbiblioteca.csp@unifesp.bropendoar:34652024-10-10T10:58:58Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false
dc.title.none.fl_str_mv GB virus type C infection modulates T-cell activation independently of HIV-1 viral load
title GB virus type C infection modulates T-cell activation independently of HIV-1 viral load
spellingShingle GB virus type C infection modulates T-cell activation independently of HIV-1 viral load
Maidana-Giret, Maria Teresa [UNIFESP]
activation
CD38
coinfection
GB virus type C
HIV-1
T lymphocyte
title_short GB virus type C infection modulates T-cell activation independently of HIV-1 viral load
title_full GB virus type C infection modulates T-cell activation independently of HIV-1 viral load
title_fullStr GB virus type C infection modulates T-cell activation independently of HIV-1 viral load
title_full_unstemmed GB virus type C infection modulates T-cell activation independently of HIV-1 viral load
title_sort GB virus type C infection modulates T-cell activation independently of HIV-1 viral load
author Maidana-Giret, Maria Teresa [UNIFESP]
author_facet Maidana-Giret, Maria Teresa [UNIFESP]
Silva, Tania M. [UNIFESP]
Sauer, Mariana M. [UNIFESP]
Tomiyama, Helena [UNIFESP]
Levi, Jose Eduardo
Bassichetto, Katia Cristina
Nishiya, Anna
Diaz, Ricardo S. [UNIFESP]
Sabino, Ester Cerdeira [UNIFESP]
Palacios, Ricardo [UNIFESP]
Kallas, Esper Georges [UNIFESP]
author_role author
author2 Silva, Tania M. [UNIFESP]
Sauer, Mariana M. [UNIFESP]
Tomiyama, Helena [UNIFESP]
Levi, Jose Eduardo
Bassichetto, Katia Cristina
Nishiya, Anna
Diaz, Ricardo S. [UNIFESP]
Sabino, Ester Cerdeira [UNIFESP]
Palacios, Ricardo [UNIFESP]
Kallas, Esper Georges [UNIFESP]
author2_role author
author
author
author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv Universidade de São Paulo (USP)
Universidade Federal de São Paulo (UNIFESP)
Publ Hlth Dept São Paulo
Fundacao Prosangue
dc.contributor.author.fl_str_mv Maidana-Giret, Maria Teresa [UNIFESP]
Silva, Tania M. [UNIFESP]
Sauer, Mariana M. [UNIFESP]
Tomiyama, Helena [UNIFESP]
Levi, Jose Eduardo
Bassichetto, Katia Cristina
Nishiya, Anna
Diaz, Ricardo S. [UNIFESP]
Sabino, Ester Cerdeira [UNIFESP]
Palacios, Ricardo [UNIFESP]
Kallas, Esper Georges [UNIFESP]
dc.subject.por.fl_str_mv activation
CD38
coinfection
GB virus type C
HIV-1
T lymphocyte
topic activation
CD38
coinfection
GB virus type C
HIV-1
T lymphocyte
description 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
publishDate 2009
dc.date.none.fl_str_mv 2009-11-13
2016-01-24T13:58:55Z
2016-01-24T13:58:55Z
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv http://dx.doi.org/10.1097/QAD.0b013e32832d7a11
Aids. Philadelphia: Lippincott Williams & Wilkins, v. 23, n. 17, p. 2277-2287, 2009.
10.1097/QAD.0b013e32832d7a11
0269-9370
http://repositorio.unifesp.br/handle/11600/31949
WOS:000271589700005
url http://dx.doi.org/10.1097/QAD.0b013e32832d7a11
http://repositorio.unifesp.br/handle/11600/31949
identifier_str_mv Aids. Philadelphia: Lippincott Williams & Wilkins, v. 23, n. 17, p. 2277-2287, 2009.
10.1097/QAD.0b013e32832d7a11
0269-9370
WOS:000271589700005
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv Aids
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 2277-2287
dc.publisher.none.fl_str_mv Lippincott Williams & Wilkins
publisher.none.fl_str_mv Lippincott Williams & Wilkins
dc.source.none.fl_str_mv reponame:Repositório Institucional da UNIFESP
instname:Universidade Federal de São Paulo (UNIFESP)
instacron:UNIFESP
instname_str Universidade Federal de São Paulo (UNIFESP)
instacron_str UNIFESP
institution UNIFESP
reponame_str Repositório Institucional da UNIFESP
collection Repositório Institucional da UNIFESP
repository.name.fl_str_mv Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)
repository.mail.fl_str_mv biblioteca.csp@unifesp.br
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