HEPATITIS-D VIREMIA FOLLOWING ORTHOTOPIC LIVER-TRANSPLANTATION INVOLVES A TYPICAL HDV VIRION WITH A HEPATITIS-B SURFACE-ANTIGEN ENVELOPE

Patients receiving orthotopic liver transplantation (OLT) because of t ype D hepatitis frequently exhibit what appears to be an autonomous, o r ''isolated,'' hepatitis D virus (HDV) infection following the transp lantation, with no evidence of hepatitis B virus (HBV) in the graft or in the serum. These observations have led to the hypothesis that HBV might not always be required for HDV infection, or that HDV could exis t as a latent infection until rescued by HBV. Alternatively, an appare ntly autonomous HDV infection could be explained by coinfection of a s mall number of hepatocytes ,vith both viruses following transplantatio n, with a very low level of HBV expression that supports low-level HDV propagation. Our results are consistent with the latter hypothesis. S ensitive polymerase chain reaction (PCR)-based analysis of HBV and HDV viremia in transplantation patients with HDV infection previously cha racterized as isolated showed that HDV viremia was not independent of HBV viremia. Additional analyses, including PCR amplification, buoyant density analysis in a CsCl gradient, and immunoprecipitation with mon oclonal hepatitis B surface antigen antibodies (anti-HBs), indicated t hat the posttransplant HDV particle is typical: it contains full-lengt h HDV RNA and an envelope of hepatitis B surface antigen (HBsAg) and i s not different from that found during the acute and chronic stages of HDV superinfection or coinfection, Moreover, an experimental test of the first hypothesis in chimpanzees did not support the idea that HDV can persist for several weeks as an isolated, latent infection that ca n be rescued subsequently by HBV. The data indicate, therefore, that l atent HDV infection is not a factor in OLT recipients. We conclude tha t the HDV virion in the posttransplantation setting is typical, and th at HDV viremia following OLT requires the helper function of HBV infec tion.