GB virus type C infection modulates T-cell activation independently of HIV-1 viral load
Autor(a) principal: | |
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Data de Publicação: | 2009 |
Outros Autores: | , , , , , , , , , |
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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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 |
_version_ |
1814268449452457984 |