Although the impact of HCV infection varies substantially between recipients, allograft failure secondary to recurrence of HCV infection is the most frequent cause of death and graft failure in HCV-infected recipients, accounting for two thirds IWR-1 mw of long term graft loss.1 Histological

features of hepatitis develop in approximately 75% of recipients in the first 6 months following liver transplantation,2 with up to 30% progressing to cirrhosis by the fifth postoperative year.2 Mortality and graft loss related to recurrence of HCV has led to long-term graft survival for recipients with HCV infection that is lower than that of recipients undergoing liver transplantation for most other indications.3 Patients who achieve sustained virological response (SVR) to treatment of posttransplant HCV infection experience less severe recurrence and lower mortality and graft loss rates than nonresponders.4-6 Although the likelihood of response to antiviral therapy varies substantially with donor and recipient IL28B genotype,7 the overall safety and efficacy of peginterferon and ribavirin in the treatment of posttransplant HCV infection are both lower than we would wish.8, 9 A recent Selleck ACP-196 prospective randomized controlled trial found that less than 60% of liver transplant recipients are able to complete peginterferon and ribavirin antiviral therapy and, on

an intention to treat basis, the SVR rate was just over 20%.10 Results of meta-analyses and single center studies are only slightly more encouraging.11, find more 12 Developing safe and effective treatment of posttransplant HCV infection is one of the most important clinical challenges in our field. It has been with

great anticipation that we have observed the steady progress of the lead candidate direct-acting antiviral agents, telaprevir and boceprevir, move through their respective clinical trial development, culminating in the Food and Drug Administration’s (FDA) approval in May of 2011. These agents offer compelling and meaningful improvements in the efficacy of treatment of genotype 1 chronic HCV infection. In the preliminary summary of the presentations for telaprevir and boceprevir the FDA Antiviral Products Advisory Committee concluded (www.FDA.gov downloads posted May 5th 2011) that for Caucasian patients who are treatment-naïve and have genotype 1 chronic HCV infection SVR rates were 75% (telaprevir) and 69% (boceprevir). For African American patients who are treatment-naïve with genotype 1 chronic HCV infection SVR rates were 65% (telaprevir) and 53% (boceprevir). Proportional increases in efficacy of these agents over peginterferon and ribavirin are even greater among treatment experienced patients. It is expected that many patients who have taken to the sidelines awaiting the routine availability of a more efficacious anti-HCV therapy will now step forward to consider treatment or re-treatment.