Total and CD5+ B cells were gradually decreased following the kinetics of the HBVDNA load after tenofovir and adefovir treatment. Upon tenofovir treatment, mTOR inhibitor the frequency of memory CD27+ B cells were increased, but absolute number declined, naïve CD27- B cells were significantly

declined in both frequency and absolute number upon tenofovir treatment. In adefovir treatment group, both naïve and memory B cells didn’t alter upon the treatment. Furthermore, CHB patients displayed higher levels of activation marker (CD69 and CD24) and tends to restored after antiviral treatment Conclusion: In conclusion, disturbed B cell homeostasis is an important feature of CHB patients and partially restore after control of viral replication by antiviral treatment. B cell antiviral MK-8669 supplier immunity is improved by restoring B cell homeostasis and activation. Key Word(s): 1. Hepatitis B virus; 2. B Cells; 3. Therapy; Presenting Author: JUNQI NIU Additional Authors: XIAOLI HU, YANFANG JIANG, YANGHANG GAO, XIAOLIN GUO, XIUMEI CHI,

HONGQING YAN Corresponding Author: XIAOLI HU Affiliations: hepatology; Central Laboratory Objective: Hepatitis C virus (HCV) infection remains a serous concern and affects 130 million people estimated in the worldwide. After exposure to HCV, about 70%–80% of people progress into chronic hepatitis C (CHC). Although antigen-specific T cells are crucial for the clearance of HCV, other immunocompetent cells also play an important role in disease progression and control. Natural killer (NK) cells play an important role in the pathogenesis and therapeutic response. Interferon-α (IFN-α) and ribavirin are the standard treatments for patients with HCV infection. This study is aimed at investigating the dynamic changes in the frequency of NK subsets following treatment in chronic hepatitis C (CHC) patients. Methods: 35 chronic HCV patient is recruited, treated with standard interferon (n = 22) and pegylated interferon

(n = 13) respectively. Frequency, phenotype and functions of NK cells in chronic HCV patients were detected by flow cytometry at baseline, 4 week, 12 week, 24 week, 48 week and 72 week. Results: CD3-CD56birght NK and CD3-CD56dimNK cell were no significant difference with health controls, while CD56birght NK was correlated with ALT, and CD56bright NK cells were significantly Ribose-5-phosphate isomerase increased after treatment. Treatment with the standard therapy increased NKp30+, NKp46+ and CD107a+ NK cells, which were positively, correlated with the declining of serum HCV-RNA, but not IFN-γ+ NK cells. Furthermore, TRAIL+ NK cell and CD107a+ NK cells were markedly increased after treatment. NKG2A+ and KIR2DL3+ NK cells were associated with early virological response (EVR) in CHC patients. Conclusion: NK cells play an important role in the pathogenesis and treatment of chronic HCV infection, IFN-α treatment promotes activation of the innate immune system, enhances its ability to clear the virus.