AIM:To evaluate the abnormal immunity and gene mutationat precore 1896 site in patients with severe hepatitis-B.METHODS:This study included 23 patients with severehepatitis-B,22 patients with acute hepatitis-B and 20 controls.Mutation at precore 1896 site of HBV gene was confirmed withrestriction fragment length polymorphism(RFLP)analysis.Cytokines including TNF-α,IFN-γ,IL-6,and IL-8 were measuredwith ELISA,and T subgroups were detected with alkalinephosphatase anti alkaline phosphatase(APAAP)technique.RESULTS:In patients with severe hepatitis-B,the infectiverate of HBV mutant strain was 52.5 %(12/23),and only onepatient with acute hepatitis-B was infected with the mutantstrain.The percentage of CD8+T lymphocyte was obviouslylower(0.16±0.02 %)and the ratio of CD4+/CD8+wasobviously higher(2.35±0.89)in mutant group than in wild-type group(0.28±0.05 % and 1.31±0.18 %,respectively,P<0.01 or P<0.05).The levels of cytokines in patients withsevere hepatitis-B were higher(TNF-α 359.0±17.2 ng/L,IFN-γ 234.7±16.5 ng/L,IL-6 347.54-31.3 ng/L,IL-8 181.1±19.6ng/L)than those in acute hepatitis-B(TNF-α 220.6±8.9ng/L,IFN-γ 174.9±12.0 ng/L,IL-6 285.8±16.5 ng/L,IL-8118.4±5.1 ng/L,P<0.01 or 0.05).In patients with severehepatitis-B,the levels of IFN-γ and IL-6 were higher in mutantgroup(273.4±26.6 ng/L,387.7±32.5 ng/L)than in wild-typegroup(207.8±12.8 ng/L,300.9±16.3 ng/L).The mortality ofpatients infected with HBV mutant strain was higher(100 %)than that with wild-type(0.9 %).CONCLUSION:In severe hepatitis-B,the infective rate ofHBV mutant strain was high.The mutant strain induces moresevere immune disorders in host,resulting in the activationof lymphocyte and release of cytokines.HBV DNA mutateseasily in response to the altered immunity.Ultimately liverdamage is more prominent. AIM: To evaluate the abnormal immunity and gene mutationat precore 1896 site in patients with severe hepatitis-B. METHODS: This study included 23 patients with severepatitis-B, 22 patients with acute hepatitis-B and 20 controls. Mutation at precore 1896 site of HBV gene was confirmed with restriction fragment length polymorphism (RFLP) analysis. Cytokines including TNF-α, IFN-γ, IL-6, and IL-8 were measured with ELISA, and T subgroups were detected with alkaline phosphatase anti-alkaline phosphatase (APAAP) technique. RESULTS: In patients with severe hepatitis-B, the infective rate of HBV mutant strain was 52.5% (12/23), and only onepatient with acute hepatitis-B was infected with the mutant strain. The percentage of CD8 + T lymphocyte was significantly lower (0.16 ± 0.02%) and the ratio of CD4 + / CD8 + was significantly higher (2.35 ± 0.89) in mutant group than in wild-type group (0.28 ± 0.05% and 1.31 ± 0.18%, respectively, P <0.01 or P <0.05). The levels of cytokines in patients with severe hepatitis-B were higher (TNF-α 359.0 ± 1 7.2 ng / L, IFN-γ 234.7 ± 16.5 ng / L, IL-6 347.54-31.3 ng / L and IL-8 181.1 ± 19.6 ng / L) than those in acute hepatitis-B / L, 174.9 ± 12.0 ng / L IFN-γ, 285.8 ± 16.5 ng / L IL-8118.4 ± 5.1 ng / L, P <0.01 or 0.05) .In patients with severehepatitis-B, the levels of IFN γ and IL-6 were higher in mutantgroup (273.4 ± 26.6 ng / L, 387.7 ± 32.5 ng / L) than in wild-typegroup (207.8 ± 12.8 ng / L, 300.9 ± 16.3 ng / L) with HBV mutant strain was higher (100%) than that with wild-type (0.9%). CONCLUSION: In severe hepatitis-B, the infective rate of HBV mutant strain was high. mutant strain induces more hormone dependent disorders in host, resulting in the activation of lymphocyte and release of cytokines. HBV DNA mutateseasily in response to the altered immunity. Ultimately liverdamage is more prominent.