HCV infection of the allograft occurs at the time of transplantation, with negative-strand HCV RNA detectable in the first postoperative week. HCV RNA is cleared rapidly from serum during the anhepatic phase. Following reperfusion, the rate of decrease in HCV RNA accelerates, almost certainly refl ecting HCV binding to its obligatory hepatic receptors. HCV RNA levels typically increase rapidly from week 2 posttransplantation, peaking by the fourth postoperative month. At the end of the first postoperative year, HCV RNA levels are, on average, 10–20-fold greater than pretransplant levels [1]. Histological features of hepatitis develop in ~75% of recipients in the first 6 months following liver transplantation [2]. By the fifth postoperative year up to 30% have progressed to cirrhosis [2]. A small proportion of patients (4–7%) develop an accelerated course of liver injury (cholestatic hepatitis C, associated with very high levels of viremia) with subsequent rapid allograft failure. Early post-LT histology, e.g., at 1 year, has been consistently predictive of subsequent fibrosis progression [1].

Antiviral therapy, HCV, Immunosuppression, Natural history, Recurrence
dx.doi.org/10.1007/978-1-4614-1192-5_22, hdl.handle.net/1765/90242
Department of Gastroenterology & Hepatology

Veldt, B.J, & Charlton, M.R. (2012). Natural history of chronic HCV after liver transplantation. doi:10.1007/978-1-4614-1192-5_22