End stage liver disease from hepatitis C is the leading indication for liver transplantation (LT) in the United States. Recurrent hepatitis C after LT is universal and causes substantial morbidity and mortality with up to 30% patients developing cirrhosis by the fifth postoperative year. Once cirrhosis is established, the risk of hepatic decompensation is approximately 40% per year. Risk factors associated with accelerated disease recurrence are elevated high viral load prior to transplantation, older donor age, prolonged ischemic time, cytomegalovirus coinfection, intensity of immunosuppression and HIV coinfection. Although the mechanisms of accelerated HCV-induced liver damage after transplantation are poorly understood, strategies employed to limit severe recurrence include avoidance of older donors, early recognition of cytomegalovirus, minimization of immunosuppression, particularly T-cell depleting therapies and pulsed steroids for acute cellular rejection. Treatment of recurrent hepatitis C post-transplant is also problematic and fraught with controversy. As there is a paucity of evidence on when treatment should be initiated, out of necessity treatment has been empiric and often varies between centers. As prophylactic treatment immediately after transplantation is rarely effective and associated with numerous side effects, most clinicians acknowledge that treatment should be initiated once early fibrosis has developed although sustained viral rates with pegylated interferon and ribavirin are frequently less than 30%. Side effects are common and can lead to dose reduction or discontinuation of treatment. For those patients who develop develop decompensated cirrhosis from recurrent hepatitis C, retransplantation may be considered.