Baron S, Dianzani F
Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston.
Antiviral Res. 1994 Jul;24(2-3):97-110. doi: 10.1016/0166-3542(94)90058-2.
Successful medical use of interferon for chronic viral infections is increasingly dependent on understanding the biologic and molecular mechanisms of the interferon system. Interferon (IFN) is one of the body's natural defenses. Production of IFN is a defensive response to foreign components of microbes, tumors and antigens. This IFN response begins with the production of the IFN proteins (alpha, beta and gamma) which then induce antiviral, antimicrobial, antitumor, and immunomodulatory actions. Thus, the initial production or administration of IFN(s) does not protect directly but instead reacts with specific receptors on cell surfaces to activate cytoplasmic transduction signals that then enter the nucleus to stimulate cellular genes encoding a number of effector proteins which lead to the defensive actions. The known molecular, humoral and cellular mechanisms by which these effector proteins exert their antiviral activities are presented. In addition, the pathogenesis of chronic infections is overviewed in the context of the interferon defenses.
干扰素在慢性病毒感染的医学应用中取得成功，越来越依赖于对干扰素系统生物学和分子机制的理解。干扰素（IFN）是人体的天然防御机制之一。干扰素的产生是对微生物、肿瘤和抗原等外来成分的防御反应。这种干扰素反应始于干扰素蛋白（α、β和γ）的产生，这些蛋白随后诱导抗病毒、抗菌、抗肿瘤和免疫调节作用。因此，最初产生或施用干扰素并不能直接提供保护，而是与细胞表面的特定受体反应，激活细胞质转导信号，这些信号随后进入细胞核，刺激编码多种效应蛋白的细胞基因，从而导致防御作用。本文介绍了这些效应蛋白发挥抗病毒活性的已知分子、体液和细胞机制。此外，还在干扰素防御的背景下概述了慢性感染的发病机制。
