Takahara T, Fukuyama Y, Saito S, Ogino T, Miyajima N, Kohase M
Department of Viral Disease and Vaccine Control, National Institute of Infectious Diseases, Tokyo 208-0011, Japan.
Jpn J Infect Dis. 1999 Apr;52(2):45-8.
The purpose of this study was to elucidate the mechanism behind low efficacy of interferon therapy to hepatitis C virus infected patients by using primary monkey hepatic parenchymal cells as a surrogate of primary human liver cells. The effects of various cytokines on the antiviral activity of IFNs in the monkey hepatic cells were studied to search for physiological inhibitors. Interleukin-1 alpha, EGF, and HGF showed suppressive effects on the antiviral activity of IFN-alpha, -beta in primary monkey hepatic cells when examined by the yield reduction method using vesicular stomatitis virus (VSV). In contrast, 50 ng/ml of TNF and IL-6 had no suppressive effect on the IFN-induced antiviral state in the hepatic cells.
本研究的目的是通过使用原代猴肝实质细胞作为原代人肝细胞的替代物,阐明干扰素治疗丙型肝炎病毒感染患者疗效低下背后的机制。研究了各种细胞因子对猴肝细胞中干扰素抗病毒活性的影响,以寻找生理抑制剂。当使用水疱性口炎病毒(VSV)通过产量减少法检测时,白细胞介素-1α、表皮生长因子(EGF)和肝细胞生长因子(HGF)对原代猴肝细胞中干扰素-α、-β的抗病毒活性表现出抑制作用。相比之下,50 ng/ml的肿瘤坏死因子(TNF)和白细胞介素-6对肝细胞中干扰素诱导的抗病毒状态没有抑制作用。