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目的：比较慢性丙型和乙型肝炎基因产物表达形态。方法：７６例经ＥＬＩＳＡ和ＨＣＶＲ－ＮＡ检测证实的ＨＣＶ肝炎活检标本，用ＮＳ３区基因克隆产物ＣＰ２２和Ｃ３３ｃ标记，并与１７６例标记ＨＢｃＡｇ的乙型肝炎比较。结果：３６例丙型肝炎的ＣＰ２２１５例胞质阳性（４１．０％），Ｃ３３ｃ１９例胞质阳性（５２．７％）。与乙型肝炎形态比较，丙型肝炎的ＣＰ２２和Ｃ３３ｃ标记随病变加重而阳性表达率升高。汇管区淋巴细胞浸润和滤泡形成、肝细胞坏死硬变、脂肪变性均有明显改变。胆管损伤和ＴＳＢ升高仅在病变加重时才超过乙型肝炎。结论：研究支持ＨＣＶ感染程度与病变程度平行的病毒直接致病机制，与乙型肝炎的间接免疫损伤机制有差异。
Objective: To compare the expression patterns of chronic hepatitis C and hepatitis B gene products. METHODS: Seventy-six HCV hepatitis biopsies confirmed by ELISA and HCVR-NA were labeled with the NS3-derived gene clones CP22 and C33c and compared with 176 HBcAg-labeled hepatitis B patients. Results: The positive cytoplasm of CP2215 in 36 cases of hepatitis C (41.0%) and the positive in cytoplasm of C33c (52.7%) in 19 cases. Compared with the hepatitis B morphology, the positive expression rates of CP22 and C33c in hepatitis C increased with the increase of the lesion. The portal area lymphocyte infiltration and follicular formation, hepatocellular necrosis, steatosis were significantly changed. Bile duct injury and elevated TSB exceed hepatitis B only as the disease progresses. Conclusions: The direct mechanism of the virus supporting the degree of HCV infection in parallel with the lesion degree is different from that of the indirect immunological damage mechanism of hepatitis B.