Katze Michael G, He Yupeng, Gale Michael
Department of Microbiology, University of Washington, Seattle, Washington 98195-8070, USA.
Nat Rev Immunol. 2002 Sep;2(9):675-87. doi: 10.1038/nri888.
The action of interferons (IFNs) on virus-infected cells and surrounding tissues elicits an antiviral state that is characterized by the expression and antiviral activity of IFN-stimulated genes. In turn, viruses encode mechanisms to counteract the host response and support efficient viral replication, thereby minimizing the therapeutic antiviral power of IFNs. In this review, we discuss the interplay between the IFN system and four medically important and challenging viruses -- influenza, hepatitis C, herpes simplex and vaccinia -- to highlight the diversity of viral strategies. Understanding the complex network of cellular antiviral processes and virus-host interactions should aid in identifying new and common targets for the therapeutic intervention of virus infection. This effort must take advantage of the recent developments in functional genomics, bioinformatics and other emerging technologies.
干扰素（IFN）对病毒感染细胞及周围组织的作用引发了一种抗病毒状态，其特征为干扰素刺激基因的表达及抗病毒活性。反过来，病毒编码了对抗宿主反应并支持高效病毒复制的机制，从而将干扰素的治疗性抗病毒能力降至最低。在本综述中，我们讨论了干扰素系统与四种具有医学重要性且具有挑战性的病毒——流感病毒、丙型肝炎病毒、单纯疱疹病毒和痘苗病毒——之间的相互作用，以突出病毒策略的多样性。了解细胞抗病毒过程和病毒-宿主相互作用的复杂网络应有助于确定病毒感染治疗干预的新的共同靶点。这项工作必须利用功能基因组学、生物信息学和其他新兴技术的最新进展。
