Pathogenesis of hepatitis C virus recurrence in the liver allograft

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Abstract
1 Hepatitis C virus (HCV) infection in the allograft occurs in the setting of greater viral burden than in nontransplantation patients. 2 Infection of the allograft occurs early (within days and possibly during the intraoperative reperfusion phase). 3 Viral burden plateaus at 1 month posttransplantation and (in the absence of cholestatic HCV) peaks at the time of acute hepatitis (1 to 4 months). 4 Acute hepatitis is associated with immune cell infiltration and hepatocyte apoptosis. 5 Cholestatic HCV seems to be a disease of direct HCV cytopathic injury in the setting of extreme virus levels, an intrahepatic T helper subtype 2 cell (TH2)‐like response, and lack of a specific HCV‐directed response. 6 Chronic hepatitic HCV seems to behave at the molecular and/or cellular level in a similar fashion to the nontransplantation setting, with activation of TH1 inflammatory, profibrotic, and proapoptotic pathways. This process operates at a greater viral burden than pretransplantation and leads to more progressive disease. 7 More studies are required to examine and distinguish allograft rejection in the setting of HCV infection from HCV infection alone.