[1] Trépo C, Chan H L, Lok A. Hepatitis B virus infection[J]. Lancet, 2014, 384(9959):2053-2063.
[2] Wang F S, Zhang Z. Host immunity influences disease progression and antiviral efficacy in humans infected with hepatitis B virus[J]. Expert Review of Gastroenterology and Hepatology, 2009, 3(5):499-512.
[3] Jiang R, Feng X, Guo Y, et al. T helper cells in patients with chronic hepatitis B virus infection[J]. Chinese Medical Journal, 2002, 115(3):422-424.
[4] Zhang Z, Zou Z S, Wang H, et al. Severe dendritic cell perturbation is actively involved in the pathogenesis of acute-on-chronic hepatitis B liver failure[J]. Journal of Hepatology, 2008, 49(3):396-406.
[5] Zhang Z, Zhang S Y, Zou Z, et al. Hyper-cytolytic activity of hepatic natural killer cells correlates with liver injury in chronic hepatitis B patients[J]. Hepatology, 2010, 53(1):73-85.
[6] Zhao J, Zhang Z, Luan Y, et al. Pathological functions of interleukin-22 in chronic liver inflammation and fibrosis with hepatitis B virus infection by promoting T helper 17 cell recruitment[J]. Hepatology, 2014, 59:1331-1342.
[7] Zhang J Y, Zhang Z, Lin F, et al. Interleukin-17-producing CD4+T cells increase with severity of liver damage in chronic hepatitis B patients[J]. Hepatology, 2010, 51:81-91.
[8] Sprengers D, van der Molen R G, Kusters J G, et al. Different composition of intrahepatic lymphocytes in the immune-tolerance and immune-clearance phase of chronic hepatitis B[J]. Journal of Medical Virology, 2006, 78(5):561-568.
[9] Zhang J Y, Zou Z S, Huang A, et al. Hyper-activated pro-inflammatory CD16 monocytes correlate with the severity of liver injury and fibrosis in patients with chronic hepatitis B[J]. PLoS One, 2011, 6(3):e17484.
[10] Zhang Z, Zhang S, Zou Z, et al. Hypercytolytic activity of hepatic natural killer cells correlates with liver injury in chronic hepatitis B patients[J]. Hepatology, 2011, 53(1):73-85.
[11] 王福生, 张纪元. HBV感染免疫应答和免疫治疗新进展[J]. 传染病信息, 2011, 24(4):193-198.
[12] Rehermann B, Nascimbeni M. Immunology of hepatitis B virus and hepatitis C virus infection[J]. Nature Reviews Immunology, 2005, 5(3):215-229.
[13] Cradick T J, Keck K, Bradshaw S, et al. Zinc-finger nucleases as a novel therapeutic strategy for targeting hepatitis B virus DNAs[J]. Molecular Therapy, 2010, 18:947-954.
[14] Bloom K, Ely A, Mussolino C, et al. Inactivation of hepatitis B virus replication in cultured cells and in vivo with engineered transcription activator like effector nucleases[J]. Molecular Therapy, 2013, 21:1889-1897.
[15] Chen J, Zhang W, Lin J, et al. An efficient antiviral strategy for targeting hepatitis B virus genome using transcription activator-like effector nucleases[J]. Molecular Therapy, 2014, 22:303-311.
[16] Bhaya D, Davison M, Barrangou R. CRISPR-Cas systems in bacteria and archaea:versatile small RNAs for adaptive defense and regulation[J]. Annual Review of Genetics, 2011, 45:273-297.
[17] Makarova K S, Haft D H, Barrangou R, et al. Evolution and classification of the CRISPR-Cas systems[J]. Nature Reviews Microbiology, 2011, 9:467-477.
[18] Cai D, Mills C, Yu W, et al. Identification of disubstituted sulfonamide compounds as specific inhibitors of hepatitis B virus covalently closed circular DNA formation[J]. Antimicrobial Agents and Chemotherapy, 2012, 56:4277-4288.
[19] Katen S P, Chirapu S R, Finn M G, et al. Trapping of hepatitis B virus capsid assembly intermediates by phenylpropenamide assembly accelerators[J]. ACS Chemical Biology, 2010, 5:1125-1136.
[20] Wang P, Naduthambi D, Mosley R T, et al. Phenylpropenamide derivatives:Anti-hepatitis B virus activity of the Z isomer, SAR and the search for novel analogs[J]. Bioorganic & Medicinal Chemistry Letters, 2011, 21:4642-4647.
[21] Stray S J, Zlotnick A. BAY 41-4109 has multiple effects on hespatitis B virus capsid assembly[J]. Journal of Molecular Recognition, 2006, 19:542-548.
[22] Gish R G, Yuen M F, Chan H L, et al. Synthetic RNAi triggers and their use in chronic hepatitis B therapies with curative intent[J]. Antiviral Research, 2015, 121:97-108.
[23] Yan H, Zhong G, Xu G, et al. Sodium taurocholate cotransporting polypeptide is a functional receptor for human hepatitis B and D virus[J]. eLife, 2012(1):e00049.
[24] Volz T, Allweiss L, Ben M M, et al. The entry inhibitor Myrcludex-B efficiently blocks intrahepatic virus spreading in humanized mice previously infected with hepatitis B virus[J]. Journal of Hepatology, 2013, 58:861-867.
[25] Lucifora J, Xia Y, Reisinger F, et al. Specific and nonhepatotoxic degradation of nuclear hepatitis B virus cccDNA[J]. Science, 2014, 343:1221-1228.
[26] Gane E J, Lim Y S, Gordon S C, et al. The oral toll-like receptor-7 agonist GS-9620 in patients with chronic hepatitis B virus infection[J]. Journal of Hepatology, 2015, 63:320-328.
[27] Al-Mahtab M, Akbar S M, Aguilar J C, et al. Therapeutic potential of a combined hepatitis B virus surface and core antigen vaccine in patients with chronic hepatitis B[J]. Hepatology International, 2013, 7(4):981-989.
[28] Akbar S M, Al-Mahtab M, Rahman S, et al. A phase Ⅲ clinical trial with a therapeutic vaccine containing both HBsAg and HBcAg administered via both mucosal and parenteral routes in patients with chronic hepatitis B[J]. Hepatology, 2013, 58(S1):647A-705A.