GB virus C (GBV-C), or hepatitis G virus (HGV), is a recently discovered enveloped RNA virus belonging to the Flaviviridae family. GBV-C/HGV is transmitted by contaminated blood and/or blood products, intravenous drug use, from mother to child, sexually, and possibly through close social contacts. Several reports indicate a high prevalence of GBV-C/HGV viremia (1-4%) within healthy populations in Europe and North America, and an even higher prevalence (10-33%) among residents in South America and Africa. GBV-C/HGV has been suggested to be a causative agent for non-A-non-E hepatitis. However, several contradictory observations suggest that its ability to cause hepatitis is questionable. Taken together most data suggest that GBV-C/HGV is not a major cause of liver disease despite recent data indicating that it may infect and replicate in hepatocytes.

GB Virus C/Hepatitis G Virus

Prevalence of GB virus type C/hepatitis G virus RNA and anti-E2 among blood donors in Southeastern France.

We evaluated in a series of 33 HCV positive (both RT-PCR and HCV RIBA 2 assays) B cell non-Hodgkin's lymphomas (NHL) patients the prevalence of active and inactive HGV infection by HGV RNA assays (RT-PCR) and anti HGV antibodies directed against E2 structural protein (immunoenzimatic method), a reliable serologic marker of past HGV infection followed by viral clearance. We found only one patient with HGV positivity at RT-PCR (3%). Twenty-six of 33 patients were positive for anti HGV/E2 antibodies (78.8%) suggesting past infection. If confirmed, our preliminary data seem to suggest a higher incidence of HGV past infection in our group of HCV positive patients with B cell NHL.

High prevalence of anti-HGV/E2 antibodies in HCV-positive patients with non Hodgkin's lymphoma

GB Virus C and Hepatitis G Virus (GBV-C/HGV) are positive, single-stranded flaviviruses. GBV-C and HGV are independent isolates of the same virus. Transmission via the blood-borne route is the commonest mode, although vertical and sexual transmission is well documented. GBV-C/HGV is distributed globally; its prevalence in the general population is 10 fold higher in African countries than in non-African countries. High prevalences of GBV-C/HGV have been found in subjects with frequent parenteral exposure and in groups at high risk of exposure to blood and blood products. The clinical significance of human infection with GBV-C/HGV is currently unclear. The virus can establish both acute and chronic infection and appears to be sensitive to interferon. Only some 12-15% of chronic Non-A, B, C hepatitis cases are infected with GBV-C/HGV. A direct association with liver pathology is still lacking and it is not yet clear as to whether GBV-C/HGV is indeed a hepatotropic virus. Current evidence suggests that the spectrum of association of GBV-C/HGV infection with extrahepatic diseases ranges from haematalogical diseases, aplastic anaemia, human immunodeficiency virus (HIV)-positive idiopathic thrombocytopenia and thalassemia, through to common variable immune deficiency and cryoglobunemia.

GB virus C/hepatitis G virus (GBV-C/HGV): still looking for a disease.

GB virus C/hepatitis G virus infection in Indian blood donors and high-risk groups

The clinical significance of GB virus C (GBV-C E2) antibody is under investigation. The prevalence rates of GBV-C RNA and antibody to GBV-C E2 glycoprotein were determined in a population of 123 Egyptian anti-hepatitis C virus (HCV)-positive patients with chronic liver disease (CLD) who had not been treated previously with interferon. Sera were tested for GBV-C RNA by the LCx assay (Abbott Laboratories, North Chicago, IL), and for GBV-C E2 antibody by enzyme immunoassay. GBV-C RNA was present in 11.4% of patients. GBV-C E2 antibody was detected in 55.9% of GBV-C RNA-negative patients and in 2.2% of GBV-C RNA-positive patients (P = 0.006). GBV-C RNA was associated significantly with a history of schistosomiasis (relative risk [RR] = 5.83, 95% confidence interval [CI] 1.99-17.14, P < 0.005) but not with parenteral risk factors. The presence of GBV-C E2 antibody was not associated with age, gender, parenteral risk factors, schistosomal infection, or HCV viremia. The HCV genotype and level of viremia were similar in GBV-C anti-E2-positive and negative patients. There was a trend toward more severe histological disease with anti-E2 seropositivity (RR = 1.45, 95% CI 0.89-2.45, P = 0.11), an association which was independent of the evidence of schistosomiasis. It is concluded that GBV-C infection is common among HCV-infected Egyptian patients with CLD due to HCV infection. A significant negative correlation between the GBV-C viremia and GBV-C E2 antibody suggests that an antibody response is associated with viral clearance. This antibody response presumably occurs spontaneously, as none of the patients had received antiviral therapy. The unexpected association between GBV-C RNA and schistosomiasis suggests that nonparenteral or occult parenteral routes of GBV-C infection are likely to be important.

Antibody to GBV-C second envelope glycoprotein (anti-GBV-C E2): is it a marker for immunity?

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Antibody to GBV-C second envelope glycoprotein (anti-GBV-C E2): is it a marker for immunity?