0001). A BAY 80-6946 mouse higher proportion of patients with HBsAg level >4.3 logIU/mL (p=0.009) and HBV DNA level ≤4.3 log IU/mL (p=0.0001) was observed in F0-1 patients. Presence of BCP variant was significantly associated with a more severe liver disease (p<0.0001). Conversely, PC variant proportion was higher in F0-1 patients. IL28B CC genotype was more frequent in patients with HBsAg level <3.3 log IU/mL (p=0.004). In mul-tivariate analysis, fibrosis stage was independently associated with age (p=0.0002), HBeAg

status (p=0.01), activity (p<0.0001) and BCP variant presence (p=0.008). The ROC analysis showed an AUC of 0.82 for the predictive model (age + HBeAg status + activity + HBeAg mutations) to identify F2-4 patients. Conclusion: Our study shows that patients with BCP variants were more at risk of cirrhosis. A strong correlation between age, activity grade, HBeAg status, HBV variants and fibrosis stage allows an accurate identification of subjects with moderate to severe liver disease who need to be treated. Our results suggest that detection of HBV variants is clinically relevant

for the assessment of the severity Wnt antagonist of HBV related liver disease. Disclosures: Olivier Lada – Grant/Research Support: Gilead Nathalie Boyer – Board Membership: MSD, JANSSEN; Speaking and Teaching: BMS Tarik Asselah – Consulting: BMS, Boehringer-Ingelheim, Roche, Merck-Schering Plough, Gilead, Janssen Patrick Marcellin – Consulting: Roche, Gilead, BMS, Vertex, Novartis, Janssen-Tibotec, MSD, Boehringer, Pfizer, Abbott, Alios BioPharma; Grant/Research Support: Roche, Gilead, BMS, Novartis, Janssen-Tibotec, MSD, Alios BioPharma; Speaking and Teaching: Roche, Gilead, BMS, Vertex, Novartis, Janssen-Tibotec, Ribonucleotide reductase MSD, Abbott The following people have nothing to disclose: Martine Lapalus, Michelle

Mar-tinot-Peignoux, Ana Carolina Cardoso, Roberto J. Carvalho-Filho, Cédric Laoué-nan, Simon Gosset, Zhang Qian, Emilie Estrabaud, Feryel Mouri Aim: The study aimed to investigate HBV rtA181T mutation profile in clinical practice and its clinical implications. Methods: Serum samples from 1 8,41 9 patients collected from July 2007 to June 2012 in Beijing 302 Hospital were investigated. Around 92% patients experienced nucleos(t)ide analogs. The rtA181T mutation and HBV genotype were determined by direct sequence analysis. Viral replication capacity, drug susceptibility and HBsAg secretion were determined in HepG2 cells that had been transfected with replication-competent HBV vectors containing reverse-transcriptase/S genes. Results: rtA181T was detected from 750 patients. The incidence escalated in the past five years (1.97%, 2.47%, 3.84%, 5.21%, and 6.35%); rtA181T emerged either alone or with other drug-resistant mutations (37.3% alone, 48.6% with adefovir-resistant mutation rtA181V/N236T, 12.1% with lamivudine-resistant mutation rtM204V/rtM204I, and 2.0% with entecavir- or multidrug-resistant mutations, respectively). In patients harboring rtA181T, 96.