The comparison of virus genome and immune reaction between asymptomatic carriers and chronic hepatitis patients infected with HBV.

从HBcAg转基因小鼠（Tg10c）和HBeAg转基因小鼠（Tg30e）脾细胞中诱导出抗原提呈细胞，HBcAg转基因小鼠具有较强的抗原提呈活性，但表达HBeAg的能力较弱，Tg10c小鼠产生抗HBcAg或HBeAg抗体的能力较低，20例无症状、肝功能无升高的无症状HBV携带者（A组）和25例HBV相关慢性肝炎患者（B组）A组患者中检测到少量突变，而B组患者中检测到多个突变。大量的突变集中在核心区域。然而，慢性B型肝炎似乎不是由特定的基因组突变或氨基酸突变引起的。在细胞因子产生测定中，B组患者的平均白细胞介素2水平高于A组患者。B组IFNγ水平高于A组。

Antigen presenting cells were induced from spleen cells of HBcAg transgenic mouse (Tg10c), or HBeAg transgenic mouse (Tg30e), and HBcAg transgenic mouse has the better ability to induce HBcAg specific antigen presenting activity, but lower ability to express HBeAg.Antibody production against HBcAg or or HbeAg was slightly low in Tg10c, and almost lost in Tg30e.20 asymptomatic HBV carrier patients (group A) who has no symptom and no elevation of liver function test and 25 HBV related chronic hepatitis patients (group B) were analyzed for virolo9ical profile and cYtokine production.Although few mutations were detected in group A patients, several mutations were found in group B patients. Lots of mutations were concentrated in the core region. However, chronic hepatitis B does not appear to be caused by a specific genomic mutation or an amino acid mutation.In the cytokine production assay, the average interleukin 2 levels were higher in group B patients than that in group A patients. Similarly, and IFNγ levels were higher in group B patients than that in group A patients.