2 or pHBC1.2. There was no difference in the number of HBc-positive cells and serum HBV-DNA levels between NOG mice transfected by pHBA1.2 and pHBC1.2 1 day after injection. Serum levels of HBV-DNA, HBs Ag and HBe Ag were detected for 3 months in NOG mice transfected pHBA1.2 and pHBC1.2, but not detectable in immune-competent Selleck Ibrutinib NOD mice 28 days after injection. NOD-scid mice showed intermediated pheno-type between NOG mice and NOD mice. These results suggested that immune response for HBV-transfected hepatocytes were

required for clearance of HBV. In contrast, all strain mice transfected with pHBA1.2 showed higher HBV-DNA levels than those transfected with pHBC1.2. Together with the finding that no difference were observed in the expression of type 1 IFN between pHBA1.2 and pHBC1.2 in any strain mice, it is suggested that mechanisms which are independent of immune response would exist for the difference in clearance between HBV genotypes. Conclusion: Although Immune system is critical for HBV clearance, the different levels of HBV viremia in genotype

A and C remains even in immune deficient mice. It is indicated that immune system is not enough for explaining the difference in HBV genotype A and C clearance. Disclosures: Tetsuo Ribociclib Takehara – Grant/Research Support: Chugai Pharmaceutical Co., MSD K.K. The following people have nothing to disclose: Yoshinobu Yokoyama, Hayato Hikita, Teppei Yoshioka, Kaori Mukai, Satoshi Aono, Takatoshi Nawa, Ryotaro Sakamori, Takuya Miyagi, Kazuyoshi Ohkawa, Naoki Hiramatsu, Tomohide Tatsumi Background: It has been reported that interferon treatment could reduce HBs

antigen (HBsAg) production in patients with chronic hepatitis B virus (HBV) infection. However, only limited selleck products HBsAg reduction is observed in patients treated with interferon therapy. One cause of this limitation may be that interferon responsiveness in human hepatocytes is suppressed by HBV infection, and, therefore, interferon stimulated genes (ISGs) are not induced sufficiently to promote anti-viral effects. In the present study, we analyzed whether the suppression of HBV replication using nucleotide analogues (NAs) could improve interferon responsiveness in HBV infected human hepatocytes. Methods: Thirty-seven chronic hepatitis B patients were enrolled. Twenty patients underwent sequential interferon therapy, which included 6 months of conventional interferon therapy, running from one month prior to discontinuation until 5 months after discontinuation of NA therapy. The remaining 17 patients underwent interferon mono-therapy. Serum HBsAg titers were measured every year for 5 years after interferon therapy. To confirm the clinical results, we performed an in vitro study using T23 cells, which were generated from HepG2 cells stably transfected with an HBV expression plasmid.