2 log IU/ml at 4 weeks); 2 patients displayed a poor decline of HCV RNA (≥ 3 log IU/ ml at 4 weeks) and stopped treatment. For baseline analysis, no cross RAVs were detected between TVR and SMV, and no correlation was observed between baseline RAVs and treatment responses. Conclusions: This study suggests that RAVs at baseline do not affect the response to SMV, Peg-IFN plus RBV. The levels of emergent RAVs decreased to low frequencies post-treatment. Disclosures: Eiji Mita – Grant/Research Support: MSD Tetsuo Takehara – Grant/Research Support: PD0325901 molecular weight Chugai Pharmaceutical Co., MSD K.K. The following people have nothing to disclose: Naoki Morishita, Naoki Hira-matsu,

Tsugiko Oze, Yuki Tahata, Naoki Harada, Ryoko Yamada, Takatoshi Nawa, Hayato Hikita, Takayuki Yakushijin, Takuya Miyagi, Yuichi Yoshida, Tomohide Tatsumi, Akira Yamada, Toshifumi Ito, Masami Inada, Yasuharu Imai, Michio Kato Background: Recurrent HCV infection following liver transplantation leads to accelerated allograft injury and is associated with reduced graft and patient survival. Therapeutic intervention with interferon is difficult

due to poor efficacy and toler-ability. The application of first generation PIs is limited due to drug-drug interactions with immunosuppressants (IS). The introduction of new IFN-free therapeutic options with DAA-com-binations are in the prospect to substantially improve the outcome for LT patients with HCV. Methods: Daclatasvir

Bortezomib research buy 60mg/ daily, simeprevir 150mg/daily and ribavirin 600mg /daily were administered as an all oral triple regimen to 6 LT patients with recurrent HCV infection, one with genotype 1a and 5 with genotype 1b. All patients were treated for 24 weeks and monitored closely concerning trough levels of IS (one received everolimus and five tacrolimus), laboratory parameters and potential side effects. Results: One patient experienced click here a viral breakthrough at treatment week (tw) 8 which was associated with emergence of resistance-associated mutations in the NS3 protease domain as well as a NS5A deletion. Antiviral regimen was successfully swiched to sofosbuvir / RBV in this case. The remaining 5 patients cleared viral load between tw 4 and 8 and achieved end of treatment response (EOT), 3 patients have a SVR4 at that stage. Clinical parameters (ALT, AST, bil-irubin, fibrosis stage) improved in all patients except a moderate transient increase of bilirubin in one. All patients tolerated the medication very well. Adverse events were hardly observed and limited to moderate anemia due to RBV. Uptake of IS and trough levels were constant during therapy, the dose of IS did not have to be adjusted. Conclusions: Our observations suggest the described regime as safe and efficient for LT patients and provide great promise for the use of this all-oral antiviral regimen in other immunosuppressed and IFN-intolerant HCV patients.