丙型肝炎病毒与I型干扰素系统的相互作用。
Interaction of hepatitis C virus with the type I interferon system.
作者信息
Weber Friedemann
机构信息
Abteilung Virologie, Institut für Medizinische Mikrobiologie und Hygiene, Universitat Freiburg, Freiburg D-79008, Germany.
出版信息
World J Gastroenterol. 2007 Sep 28;13(36):4818-23. doi: 10.3748/wjg.v13.i36.4818.
Abstract
Hepatitis C virus (HCV) needs to tightly manipulate host defences in order to establish infection. The innate immune response slows down viral replication by activating cytokines such as the type I interferons (IFN-alpha/beta), which trigger the synthesis of antiviral proteins and modulate the adaptive immune system. HCV has therefore developed a number of countermeasures to stay ahead of the IFN system. Here, I will attempt to summarize the current state of research regarding IFN responses against HCV and the viral escape strategies. Particular emphasis will be put on the newly discovered mechanisms HCV employs to avoid the induction of IFN in infected cells.
摘要
丙型肝炎病毒（HCV）为建立感染需要紧密操控宿主防御机制。先天性免疫反应通过激活诸如I型干扰素（IFN-α/β）等细胞因子来减缓病毒复制，这些细胞因子会触发抗病毒蛋白的合成并调节适应性免疫系统。因此，HCV已开发出多种对策以领先于干扰素系统。在此，我将尝试总结关于针对HCV的干扰素反应及病毒逃逸策略的当前研究状况。将特别着重于HCV用于避免在受感染细胞中诱导干扰素的新发现机制。
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