C型肝炎病毒感染後會造成慢性C型肝炎,而且與肝硬化及肝癌的形成有關,是目前全世界相當重視的病毒之一。在慢性C型肝炎患者體內發現,腫瘤壞死因子.alpha.(Tumor necrosis factor-.alpha.;TNF-.alpha.)會比正常人分泌量高。TNF-.alpha.可能在肝炎的肝臟病理變化中具有重要的意義,也和干擾素治療慢性C型肝炎的效果有關。C型肝炎病毒感染後,我們認為病毒基因產物可能是調控TNF-.alpha.表現的重要因子之一,於是本實驗我們選擇病毒蛋白質中,具有基因調控功能的核心蛋白質進行研究。我們共同轉染核心蛋白質載體,與以TNF-.alpha. promoter連接CAT基因的載體,轉染至T細胞株H9細胞以及肝癌細胞株Huh7細胞,由CAT assay的結果發現,C型肝炎病毒核心蛋白質不能活化TNF-.alpha. promoter的活性,所以目前沒有證據顯示核心蛋白質能調控TNF-.alpha.的基因表現,但是否可經由C型肝炎病毒其他基因產物來調控,有待更多實驗證明。 The immunoregulatory cytokines may be important in the host response to hepatitis C virus infection. Among cytokines, tumor necrosis factor-.alpha. (TNF-.alpha.) has been involved in the pathogenesis of diversity of liver condition including viral hepatitis. The Aims of this study is to investigate whether the HCV core protein could regulate the expression of TNF-.alpha. gene. In this study, H9 cells and Huh-7 cells were cotransfected with TNF-CAT construts and HCV core effector plasmids, and a transient transfection assay to determine whether the viral protein regulated expression of the TNF gene. No TNF-.alpha. promoter activity was noted in the present of the core effector plasmids in two cell lines. These studies suggested that activation of TNF gene expression may be affected by other gene products or not associated with any viral products of HCV.
