HGV GBV-C INFECTION IN LIVER-TRANSPLANT RECIPIENTS - ANTIBODIES TO THE VIRAL E2 ENVELOPE GLYCOPROTEIN PROTECT FROM DE NOVA INFECTION/

Background/Aims: Liver transplantation for endstage liver cirrhosis pr ovides a useful model to investigate the pathogenetic role of hepatotr opic viral agents. Recently, a new member of the Flaviviridae family, provisionally named HGV/GBV-C virus, has been associated with acute an d chronic non A-E hepatitis. We studied 136 patients with cirrhosis co nsecutively 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 transplanta tion (median follow-up 44 months) and underwent routine liver biopsies . Hepatitis G virus infection was studied using both direct viral RNA identification by RT-PCR and indirect detection of antibodies to the E 2 glycoprotein. Results: There was a high frequency of the hepatitis G virus among patients undergoing liver transplantation, with HGV RNA a nd anti-E2 prevalence rates of 18.4% and 26.5%, respectively, HGV RNA prevalences significantly increased after transplantation (47.8%), wit h 47.3% rate of new infections in susceptible subjects. Anti-E2 antibo dies were significantly more prevalent among patients transplanted for HCV-related cirrhosis and represented a strong protective factor agai nst hepatitis G virus reinfection or recurrent infection, No correlati on 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 a re heavily exposed to hepatitis G virus both before and after transpla ntation, hepatitis G virus does not induce liver disease in this setti ng. Most infections appear to be self-limited and induce a protective immunity which is marked by the presence of anti-E2 antibodies.