Disease relevance of GB virus C

• HIV replication, as measured by the detection of p24 antigen in culture supernatants, was reproducibly inhibited in cultures of peripheral-blood mononuclear cells by GBV-C coinfection [1].
• Among the 400 adults who underwent cardiac surgery, 40 were positive for GBV-C RNA, including six whose pretransfusion sera were already positive and seven coinfected with hepatitis C virus (HCV) during transfusion [2].
• Although GBV-C is not yet associated with any cause of liver disease, a humoral immune response against the GBV-C envelope 2 (E2) protein has been observed [3].
• Our data indicate that GBV-C does not cause chronic hepatitis in immunocompromised XLA patients and is not the cause of chronic non-B or -C hepatitis in the majority of CVID patients [4].
• The high prevalence of GBV-C viremia in CVID and XLA patients is probably explained by their long-term exposure to blood products [4].

Psychiatry related information on GB virus C

• Patients were evaluated based on past history, present illness, history of habitual alcohol consumption, results of the serological and biochemical laboratory tests at diagnosis of HCC, Anti-HBc antibody, autoantibodies, GBV-C/HGV RNA, and histopathologic findings of non-cancerous portion of the liver were also evaluated [5].

High impact information on GB virus C

• RESULTS: Genomic GBV-C RNA was found in 10 of 56 (18%) of the sera [6].
• We investigated six cases of fulminant hepatitis of unknown aetiology for the presence of GBV-C genome in their serum, and three showed positive signals by semi-nested PCR using primers derived from the NS3/helicase region [7].
• MEASUREMENTS: GB virus C RNA was determined by a reverse-transcription polymerase chain reaction assay done by using primers derived from the conserved GBV-C helicase region [8].
• However, no evident symptoms or signs were noted in the 25 patients infected by GBV-C alone, and the average peak serum alanine aminotransferase activity was 31 IU/L only (range, 12 to 123), with persistently normal levels in 20 patients [2].
• Therefore, we studied the prevalence and clinical relevance of GBV-C RNA and anti-E2 antibodies in patients undergoing orthotopic liver transplantation (OLT) [3].

Chemical compound and disease context of GB virus C

• AIMS: To retrospectively investigate the possible relation between the presence of GBV-C markers (RNA or antibodies to the GBV-C envelope 2 (E2) glycoprotein) and FHF [9].
• In addition, two types of GBV-C particles were identified in cell lysates; these particles had buoyant densities of 1.06 and 1.12 to 1.17 g/ml in sucrose gradients [10].
• Interferon-alpha treatment caused a marked but usually transient reduction in serum GBV-C/HGV RNA, and ribavirin had, at most, a modest antiviral effect [11].
• Prevalence of GB virus type C/hepatitis G virus RNA and of anti-E2 in individuals at high or low risk for blood-borne or sexually transmitted viruses: evidence of sexual and parenteral transmission [12].
• Importantly, GBV-C/HGV co-infection was not associated with any changes in indices of liver diseases, including serum alanine transaminase levels, Knodell score or histology activity index (HAI) [13].

Biological context of GB virus C

• To study the existence of GB virus C/hepatitis G virus (GBV-C/HGV) variants with different tropism, we have analyzed the heterogeneity and quasispecies composition of GBV-C/HGV isolated from in vitro-infected peripheral blood mononuclear cells (PBMC) and from sera, livers, and PBMC from two chronically infected patients [14].
• However, these genomic GBV-C RNA sequences differed in the NS3 (helicase) region from the genomic RNA isolated from the GBV-C prototype previously reported by Simons et al [15].
• Slower progression was not related to polymorphisms in CCR genes, HLA genotype, or GB virus C coinfection [16].
• Genetic diversity between hepatitis G virus isolates: analysis of nucleotide variation in the NS-3 and putative 'core' peptide genes [17].
• These data indicate that clinical GBV-C isolates vary in their ability to persist in culture, do not require PHA/IL-2 stimulation, and that sequence variability in key regulatory regions may affect growth in PBMC cultures [18].

Anatomical context of GB virus C

• CONCLUSIONS: CD4 and CD8 T lymphocytes are stimulated by GBV-C to secrete antiretroviral factors, inhibiting R5- and X4-HIV strains [19].
• High homologous nucleotide to GBV-C was amplified from DNA of MT2 and HeLa cells and PBMC of human and chimpanzee [20].

Gene context of GB virus C

• Inhibition of HIV-1 replication by GB virus C infection through increases in RANTES, MIP-1alpha, MIP-1beta, and SDF-1 [21].
• Regulation of CC chemokine receptor 5 in hepatitis G virus infection [22].
• In contrast to the findings of ex vivo analysis, no statistically significant differences were observed in levels of CCL5, stromal cell-derived factor 1, interleukin-7, and tumor necrosis factor-alpha in plasma of patients with or without GBV-C viremia [23].
• To explore the approaches and mechanisms for reversing the immune tolerance in transgenic mouse, and the pathogenicity of hepatitis G virus (HGV), the promoter of phoP-activated gene (P(pagC)) of Salmonella typhimurium was used as a transcriptionally regulating element to construct an attenuated S. typhimurium expressing HGV NS3 [24].
• In addition, we tested whether the prevalence of anti-E2 antibodies may protect against GBV-C infection [3].

Analytical, diagnostic and therapeutic context of GB virus C

• Antibodies to GBV-C in serum samples were detected by enzyme immunoassay based on a recombinant GBV-C E2 protein [9].
• The viral E2 antigen was detected by immunofluorescence in the cells inoculated with the fifth passage of GBV-C [25].
• Additional sera were available for GBV-C RNA testing in 465 of 573 (81%) patients, and GBV-C RNA was detected by RT-PCR in 146 [26].
• Antibodies to the E2 protein of hepatitis G virus were detected by means of an enzyme-linked immunosorbent assay [27].
• HGV/GBV-C infection in liver transplant recipients: antibodies to the viral E2 envelope glycoprotein protect from de novo infection [28].

References