E. Silini et al., HGV GBV-C INFECTION IN LIVER-TRANSPLANT RECIPIENTS - ANTIBODIES TO THE VIRAL E2 ENVELOPE GLYCOPROTEIN PROTECT FROM DE NOVA INFECTION/, Journal of hepatology, 29(4), 1998, pp. 533-540
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.