No study has examined the role of EGF genotype, and only one study has examined the role of PNPLA3 genotype in LT recipients. IL28B genotype is associated with IFN-based treatment response in LT recipients, although data differ regarding its association with allograft disease course. We

sought to determine whether these SNPs predict cirrhosis development and graft survival in a multicenter population. Methods: HCV Erlotinib patients who underwent LT at MGH, Beth Israel Deaconess, and Lahey Clinic between 1990 and 2008 were studied. Genotypes were determined from donor wedge or allograft biopsies and recipient explants. Cox proportional hazards regression model was used to assess time to cirrhosis, liver-related death, and re-LT, adjusting for donor age and sustained virologic response (SVR) as a time-dependent covariate. Logistic regression was used to assess SVR in patients receiving antiviral therapy. Results: The cohort comprised 257 LT recipients followed for a median of 6.9 years. We observed a trend towards a higher rate of progression

to cirrhosis among recipients with an EGF non-AA vs. AA donor genotype (adjusted HR 2.02; 95%CI 0.93–4.37; p=0.07). No association was observed between recipient EGF, IL28B, and PNPLA3 or donor IL28B and PNPLA3 genotypes and cirrhosis. Additionally, no association was observed between these genotypes and graft survival. Among treated patients, the presence of

the CC IL28B variant in either the recipient (R) or donor (D) liver was associated with increased rate of SVR Maraviroc cost (R-CC/D-CC 8/12 [67%], R-non-CC/ D-CC 19/42 [45%], R-CC/D-non-CC 3/9 [33%], R-non-CC/D-non-CC 12/45 [27%], p=0.07). Conclusions: Recipient EGF, IL28B, and PNPLA3 and donor IL28B and PNPLA3 genotypes do not predict adverse outcomes in LT recipients with HCV. www.selleck.co.jp/products/Romidepsin-FK228.html A potential association exists between donor EGF genotype and cirrhosis. Since the EGF GG genotype produces higher serum and liver levels of EGF than the non-GG genotype, and since the EGF receptor is involved in HCV entry, this finding is biologically plausible. Future efforts will be directed at investigating this relationship in larger cohorts. The results also suggest that IL28B and PNPLA3 genotypes do not play a major role in determining the natural history of allograft hepatitis C. Disclosures: Jessica L. Mueller – Employment: NIDDK Kathleen E. Corey – Advisory Committees or Review Panels: Gilead; Speaking and Teaching: Synageva Kenneth K. Tanabe – Patent Held/Filed: EGF SNP and risk for HCC, EGFR inhibition and HCC, gene signature for prognosis in cirrhosis Michael P. Curry – Grant/Research Support: Gilead Sciences, Mass Biologics, Merck, Salix, Conatus; Stock Shareholder: Achilion, Idenix Raymond T.