Cirrhosis due to hepatitis C (HCV) is now the most common indication for liver transplantation in western Europe and the United States. Given the absence of effective prophylaxis, recurrent HCV infection is almost inevitable. Although the natural history and outcome of recurrent HCV infection are now better documented, the factors which influence the recurrence of hepatitis and its subsequent progression are still unclear.1 In fact, the variation in the consequences of liver disease associated with recurrent HCV infection suggest that several viral and host factors are important in determining clinical outcome. Despite the rapid growth in knowledge of the molecular biology of hepatitis C, our understanding of the immunopathology of chronic HCV infection is still poor. Immunosuppression may well be the single most important factor responsible for variations in clinical outcome. Evidence of its potential involvement includes a more aggressive histological picture in non-transplanted patients with congenital or acquired immunodeficiency2 ,3 as well as among liver transplant recipients who require treatment with steroid boluses for acute rejection.4 In the transplant setting, however, there are conflicting reports of …