Navegando por Palavras-chave "GB virus C"
Agora exibindo 1 - 3 de 3
Resultados por página
Opções de Ordenação
- ItemAcesso aberto (Open Access)Analysis of GB virus C infection among HIV-HCV coinfected patients(Sociedade Brasileira de Medicina Tropical - SBMT, 2009-10-01) Barbosa, Aline de Jesus [UNIFESP]; Baggio-Zappia, Giovana Lotici [UNIFESP]; Dobo, Cristine [UNIFESP]; Alves-Sousa, Viviane Kelly [UNIFESP]; Lanzara, Graziela de Almeida [UNIFESP]; Silva, Ismael Dale Cotrim Guerreiro da [UNIFESP]; Lanzoni, Valeria Pereira [UNIFESP]; Granato, Celso Francisco Hernandes [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)The aim of this study was to evaluate the effect of GB virus C on laboratory markers and histological parameters among HIV-seropositive patients coinfected with HCV. Lower degrees of hepatic lesions were observed in the triple-infected patients, in comparison with HIV-HCV coinfected patients who were negative for GBV-C RNA.
- ItemAcesso aberto (Open Access)Avaliação de parâmetros da resposta imunológica na co-infecção pelo HIV-1 e vírus das hepatites C e G (HGV/GBV-C)(Universidade Federal de São Paulo (UNIFESP), 2009-06-24) Baggio-Zappia, Giovana Lotici [UNIFESP]; Granato, Celso Francisco Hernandes [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)GBV-C co-infection is frequent in humans and could last for years without clinical symptoms. GBV-C is a flavivirus composed by a single positive RNA strain, closely related to HCV. Initially in its discovery GBV-C was associated with non-A-B hepatitis. However, subsequent studies failed to associate GBV-C with any known human disease and the virus became neglected until a series of studies associated the virus with prolonged survival in HIV infected recipients. Studies evaluating the co-infection presents conflicting results whereas triple HIV-HCV-GBV-C infection remains to be clarified. With the aim to evaluate the effect of GBV-C upon HIV and HIV-HCV co-infected patients, we included a cohort of 159 HIV-seropositive patients from CCDI-UNIFESP. The patients were tested for the presence of anti-E2 antibodies and GBV-C RNA. Of the 107 HIV seropositive patients negative to HCV infection, 41 (38,3%) were positive to GBV-C infection markers, of whom 17 (15,8%) were GBV-C viremic and 24 (22,4%) were positive to anti-E2 antibodies. Of the 52 HIV-HCV co-infected patients, 24 (46,1%) were positive to GBV-C infection markers, of whom 14 (26,9%) were viremic and 10 (19,2%) presented anti-E2 antibodies. Epidemiological data were collected; virological and immunological markers and also hepatic function were evaluated. Besides, IFN- and IL-2 production on CD4, T CD8 and T cells and CD38 activation marker on T CD4 and T CD8 cells were also evaluated. No significant differences on HIV viral load nor on T CD4 and T CD8 cell counts were observed, according to the infection profile. Immune response, evaluated by the IFN- and IL-2 production and by the CD38 expression did not differ among the groups studied. Univariate analysis demonstrated higher ALT, AST and GGT levels in the HIV-HCV co-infetced and HIVHCV- GBV-C triple infected patients. The multivariate analysis demonstrated that the GBV-C influences ALT levels on triple infected patients. Our results demonstrate that GBV-C does not exerts beneficial effects upon chronically HIV infected patients, unlike, it can cause hepatic overload, as demonstrated by the higher ALT levels in the HIV-HCV-GBV-C triple infected patients. In the light of these results, is reasonable to prudently consider this interaction until the possible pathological role of GBV-C on this situation is completely excluded.
- ItemSomente MetadadadosHIV-GB virus C co-infection: an overview(Walter de Gruyter & Co, 2009-01-01) Baggio-Zappia, Giovana Lotici [UNIFESP]; Hernandes Granato, Celso Francisco; Universidade Federal de São Paulo (UNIFESP); Fleury Med & HlthGB virus C (GBV-C) and hepatitis G virus (HGV) are two isolates of the same virus, independently identified in humans in the 1990s by two research laboratories, and were initially considered a potential cause of liver disease. Studies failed to associate the virus with hepatitis or any known human disease. GBV-C reappeared in the scientific scene when some research groups, in an attempt to find the interference of the virus among HIV seropositive patients, reported a lower mortality rate and slower disease progression among co-infected patients. From then on, several mechanisms have been proposed to clarify this putative benefit; however, the question whether GBV-C exerts a protective effect in HIV-infected patients remains to be resolved.