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Control of hepatitis in the transplant patient: a journey begun – but not there yet

Since the earliest days of successful renal transplantation, chronic liver disease has been observed in 10–15% of recipients. Initially, hepatitis B virus (HBV) was a major cause of this disease; with the advent of sensitive methods for testing blood and organ donors, and effective infection control methods in dialysis units and in hospitals, hepatitis B was replaced by non-A, non-B hepatitis as the major cause of chronic liver disease, still with an incidence of 10–15%. Today, we know that the great majority of cases of non-A, non-B hepatitis are due to hepatitis C virus (HCV), but chronic liver disease in transplant patients remains a significant problem (1, 2). As a general rule, post-transplant immunosuppression will amplify the extent of hepatitis viral replication, increase the incidence and severity of clinical syndromes, encourage the persistence of chronic viral replication, and shorten the duration of time necessary for the development of end-stage liver disease and/or hepatocellular carcinoma. In this issue of Transplant Infectious Disease, the current status of HBV and HCV, as they affect transplant patients, is presented (3–5). The amplification of HBV and HCV replication with the initiation of post-transplant immunosuppression is well documented (3, 4); the uncommon but clinically severe form of clinical disease produced by both viruses, fibrosing cholestatic hepatitis, is defined (5); the acceleration of the effects of chronic viral replication in transplant leading to cirrhosis and hepatocellular carcinoma are delineated; and the special problems of the liver allograft recipient are outlined (3–5). On a positive note, not only is the molecular pathogenesis of HBV and HCV being unraveled, and the risk of transmission at the time of transplant being reduced, but therapies effective in transplant patients are beginning to emerge – hepatitis B immunoglobulin and lamivudine for HBV, and the combination of interferon and ribavirin for HCV. Despite these advances, problems remain with currently available therapies. It is now apparent that extended therapy will be necessary in transplant patients, due not only to the nature of these viral infections but also to the ongoing amplifying effects of chronic immunosuppression. In HBV infection, chronic therapy with lamivudine will lead to the eventual emergence of re-