HGV-GBV-C infection in liver transplant recipients. Antibodies to the viral E2 envelope glycoprotein protect from de novo infection

BACKGROUND/AIMS: Liver transplantation for endstage liver ricchosis provides a useful model to investigate the pathogenetic role of hepatotropic viral agents. Recently, a new member of the Flaviviridae family, provisionally named HGV/GBV-C virus, has been associated with acute and chronic non A-E hepatitis. We studied 136 patients with cirrhosis consecutively transplanted at our institution for evidence of hepatitis G virus infection and correlation with the patients' clinical course. METHODS: All patients survived for at least 6 months after transplantation (median follow-up 44 months) and underwent routine liver biopsies. Hepataitis G virus infection was studied using both direct viral RNA identification by RT-PCR and indirect detection of antibodies to the E2 glycoprotein. RESULTS: There was a high frequency of the hepatitis G virus among patients undergoing liver transplantation, with HGV RNA and anti-E2 prevalence rates of 18.4% and 26.5%, respectively, HGV RNA prevalences significantly increased after transplantation (47.8%) with 47.3% rate of new infections in suceptible subjects. Anti-E2 antibodies were significantly more prevalent among patients transplanted for HCV-Related cirrhosis and represented a strong protective factor against hepatitis G virus reinfection or recurrent infection. No correlation was found between HGV RNA or anti-E2 prevalences and survival after transplantation or rates of recurrent liver damage. CONCLUSIONS: All available evidence suggests that, although liver transplant patients are heavily exposed to hepatitis G virus both before and after transplantation, hepatitis G virus does not induce liver disease in this setting. Most infections appear to be silf-limited and induce a protective immunity which is marked by the presence of anti-E2 antibodies.