Human leukocyte antigen class I‐independent pathways may contribute to hepatitis B virus‐induced liver disease after liver transplantation

Abstract

The proliferative response of peripheral blood lymphocytes to the HBcAg was compared with serological, molecular and immunohistochemical parameters of hepatitis B virus infection and with biochemical and histological parameters of liver disease in a patient who received a completely human leukocyte antigen class I‐mismatched liver allograft for fulminant hepatitis. The proliferative response increased progressively after transplantation, as hepatitis B virus infection became reestablished in the hepatic allograft. Strikingly, the HBcAg‐specific T cells suddenly disappeared from the peripheral blood immediately before the acute onset of a severe necroinflammatory liver disease in which more than 80% of the hepatocytes expressed HBcAg. These observations are compatible with the hypothesis that human leukocyte antigen class I‐independent hepatitis B virus‐specific T cells might play a previously unsuspected role in the pathogenesis of hepatitis B virus‐induced liver disease. (HEPATOLOGY 1993;18:491–496.) Copyright © 1993 American Association for the Study of Liver Diseases