Ribavirin in the treatment of recurrent hepatitis C after liver transplantation: Difficult to manage but essential for success

HCV-related cirrhosis is currently the leading indication for liver transplantation in Europe and in the USA [1,2]. HCV recurrence after transplantation is almost universal and 60–90% of patients will develop lesions of chronic hepatitis C on the graft [3]. The course of HCV graft disease is accelerated in transplant recipients compared to immune competent patients, with reported incidence rates of cirrhosis at 5 years of approximately 10–30% [3–5]. This results in an excess risk of death or re-transplantation for liver failure at 10–15 years posttransplant [2,6]. The reasons for this accelerated course are incompletely understood. Several factors are involved: viral-related (genotype, viral load, quasispecies selection), immunological in nature (immunosuppression, quality and intensity of immune response) as well as related to the liver graft itself (quality of the graft, age of the donor). Two main types of chronic graft lesions have been described. The first, named fibrosing cholestatic hepatitis (FCH), is rare and severe. FCH usually occurs during the first post-transplant year, represents 10% of the cases of post-transplant hepatitis, and is characterized by the association of jaundice and liver failure [7]. FCH appears to arise from the inability of the immune system of the recipient to clear HCV from the liver, leading to a high amount of HCV in the graft associated with a stable HCV quasispecies [8]. It has therefore been suggested that, in this particular context