OBJECTIVES: To investigate the prevalence of GB virus C (GBV-C)/hepatitis G virus (HGV) RNA and anti-E2 antibodies in different risk groups of HIV-infected patients compared to that in healthy blood donors, and to study the effects of possible interactions between HIV and GBV-C/HGV on the carrier state and hepatic changes. METHODS: Sera from 100 consecutive unselected HIV-infected outpatients and from 100 healthy blood donors were screened for GBV-C/HGV viremia and anti-E2 antibodies. Anti-E2 antibodies were detected using an immunoassay developed by Boehringer Mannheim according to the manufacturer's instructions. GBV-C/HGV RNA was extracted from sera and reverse transcribed. The resulting cDNA was amplified with a PCR developed in the laboratory with primers derived from the 5prime prime or minute noncoding region of the viral genome and detected with a specific capture probe. This procedure was validated by a French multicenter quality control group. RESULTS: Thirty-one of the 100 HIV-infected patients and 8% of the healthy blood donors displayed anti-E2 antibodies. Four HIV-infected patients and one healthy blood donor were found to be GBV-C/HGV viremic. When analyzed by risk factor for the acquisition of HIV, no differences in the prevalence of anti-E2 antibodies were found between intravenous drug users and homosexual and heterosexual patients. CONCLUSIONS: We found a high prevalence of GBV-C/HGV infection in the HIV-infected population, irrespective of the risk group factor for HIV infection, suggesting that the sexual route is as effective as the parenteral route for the acquisition of GBV-C/HGV. No biological alteration could be attributed to GBV-C/HGV, even in the viremic patients. HIV-infected patients were able to clear GBV-C/HGV viremia and to mount a humoral immune response.
OBJECTIVES: To investigate the prevalence of GB virus C (GBV-C)/hepatitis G virus (HGV) RNA and anti-E2 antibodies in different risk groups of HIV-infectedpatients compared to that in healthy blood donors, and to study the effects of possible interactions between HIV and GBV-C/HGV on the carrier state and hepatic changes. METHODS: Sera from 100 consecutive unselected HIV-infected outpatients and from 100 healthy blood donors were screened for GBV-C/HGV viremia and anti-E2 antibodies. Anti-E2 antibodies were detected using an immunoassay developed by Boehringer Mannheim according to the manufacturer's instructions. GBV-C/HGV RNA was extracted from sera and reverse transcribed. The resulting cDNA was amplified with a PCR developed in the laboratory with primers derived from the 5prime prime or minute noncoding region of the viral genome and detected with a specific capture probe. This procedure was validated by a French multicenter quality control group. RESULTS: Thirty-one of the 100 HIV-infectedpatients and 8% of the healthy blood donors displayed anti-E2 antibodies. Four HIV-infectedpatients and one healthy blood donor were found to be GBV-C/HGV viremic. When analyzed by risk factor for the acquisition of HIV, no differences in the prevalence of anti-E2 antibodies were found between intravenous drug users and homosexual and heterosexual patients. CONCLUSIONS: We found a high prevalence of GBV-C/HGV infection in the HIV-infected population, irrespective of the risk group factor for HIV infection, suggesting that the sexual route is as effective as the parenteral route for the acquisition of GBV-C/HGV. No biological alteration could be attributed to GBV-C/HGV, even in the viremic patients. HIV-infectedpatients were able to clear GBV-C/HGV viremia and to mount a humoral immune response.
Authors: John D Kriesel; Maurine R Hobbs; Brandt B Jones; Brett Milash; Rashed M Nagra; Kael F Fischer Journal: PLoS One Date: 2012-03-08 Impact factor: 3.240