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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.