RESULTS: NS3 mutations V36L (N=2), T54S (N=6), Q80K (N=1), S138L (N=1), D168E (N=3), V170L (N=1),

and V36I+Q80R (N=1) were detected and mutation rate was 7.2%. R155K and A156V which are lead to a high level resistance to NS3 inhibitors were not detected. NS5A mutations L31M (N 8), L31V (N=1),Q54H (N=42), Q54P (N=2), Q54K (N=1), Q54L (N=1), Q54N (N=2), Q54S (N=1), Q54Y (N=3), Q62E (N=2), Q62H (N=1), Q62N (N=1), Q62S (N=4), Y93H (N=7), L31I+Q54H (N=1), L31M+Q54H (N=2), Q54H+Q62E (N=8), Q54H+Q62A (N=3), Q54H+Y93H (N = 10), and L31M+Q54H+Y93H (N = 1) were detected and mutation rate was 48.3%. L31M and Y93H which associated with high level resistance to NS5A inhibitors were frequently found. NS5B mutations C316N (N=54), M414L (N=2), Y448N (N=2), Peptide 17 chemical structure and C316N+Y448N (N=1) were detected and mutation rate was 28.5%. S282T which is RAV for nucleoside NS5B inhibitor was not found. 8 patients simultaneously have RAV in both NS3 and NS5A

regions and 12 patients simultaneously have RAV in both NS5A and NS5B regions. CONCLUSIONS: The preexisting RAV for NS5A inhibitors click here and nonnucleoside NS5B polymerase inhibitors are frequently found but the naturally occurring resistance mutations against 2nd generation of NS3 protease inhibitors and nucleoside NS5B polymerase inhibitors are rare. These results indicated that the combination of 2nd generation of NS3 protease and nucleoside NS5B polymerase inhibitors would be optimal IFN free regimen. Disclosures: Hidemi Goto – Grant/Research Support: MSD, Roche, Bayer, Bristol-Myers, Eisai, Ajinomoto, Otsuka, Astra, Tanabe The following people have nothing to disclose: Kazuhiko Hayashi, Masatoshi Ishigami, Yoji Ishizu, Teiji Kuzuya, Takashi Honda, Yoshiaki Katano, Yoshiki Hirooka Hepatitis C virus (HCV) is phylogenetically divided into multiple genotypes and subtypes, owing to their extreme genetic diversity. Different geno/subtypes may display different replicative capacity, immunologic escape, and resistance against direct-acting antivirals (DAA). Co-existence of different geno/ subtypes may be found in patients

with blood transfusion, organ transplantation, or intravenous drug use. The prevalence of co-existence and its clinical significance, however, have not been fully elucidated. To investigate the prevalence of HCV infection with MCE公司 multiple geno/subtypes among HCV/HIV co-infected hemophiliac and HCV mono-infected post-transfusion patients, twenty one HCV positive sera (eleven HCV/HIV co-infected and ten HCV mono-infected) were collected. HCV E1-NS3 fragments were amplified by RT-PCR, and analyzed via direct sequencing (DS) and next-generation sequencing (NGS). In NGS experiments, viral haplotypes were computationally reconstructed using previously published program. The detection limit (0.01%) was preliminary determined from simulations and control experiments.