关键词：hepatitis B virus chronicity activation-induced cell death (AICD) muitldrug resistance(MDR) mutation
Abstract In recent years， people have makeda great deal of investigation on and gained remarkable insight into the mechanism ofchronicity of HBV infection, including ：①HBV antigen-specific cytotoxic T cel1s (CTL)undergo"activation-induced cell death (AICD)"more severely than usua1，so theycan't eradicate HBV infected target cells ；②these CTL can also damage other immuneactive cel1s and contribute to forming wide immunosupression in hosts ；③ the balancebetween Th1 and Th2 cells' response may be disturbed ；④ gene mutation and/orexpression deficiency of antiviral cytokines and their receptors have occurred ；⑤antigenpresenting cells(APC) process and present viral antigens deficient1y; ⑥somecirculating immune complexes (CIC) may contribute to chronicity of HBV infection；⑦hepatocytes can't execute ful1y their cooperative function in immune response andregulation ；⑧ HBV-specific T cells have suffered clonal deletion during the ontogenyperiod ；⑨ HBxAg can trans-activate the human multidrug resistance (MDR)-1 gene andassociated genes ；andmutation of viral genome and antigen have emerged under host'simmune pressure. In this review, we have discussed all these items and pointed out thatthere still have many other questions to be researched and clarified.
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