Planz Oliver
Friedrich-Loeffler-lnstitut, Bundesforschungsinstitut für Tiergesundheit, Institut für Immunologie,Tübingen, Germany.
Berl Munch Tierarztl Wochenschr. 2006 Mar-Apr;119(3-4):101-11.
It has been described in the last years that after influenza virus-infection a variety of intracellular signalling pathways have been induced. There are examples and suggestions how the viral replication cycle leads to the activation of intracellular signalling pathways. A variety of signalling pathways are activated after virus-infection as an alert-response against the invading pathogen that can be considered as an antiviral response of the host cell. Nevertheless, it was also shown, that viruses are able to suppress these cellular responses to assure their own replication. Moreover, viruses are also able to activate and misuse cellular signalling pathways for their own survival. The NF-kappaB signalling pathway is an excellent example of these sceneries. Activation of the NF-kappaB signalling pathway mediated by the virus can partially be blocked by the NS1 protein to suppress a strong antiviral IFN alpha/beta response. At the same time the virus takes advantage of the remaining NF-kappaB activity for virus related apoptosis and for its own replication. This is a highly effective and economic way for the virus to control its replication without the need for specific viral inducers of cellular responses. This demonstrates, that there are no "all or nothing" reactions in the field of interactions of Influenza viruses with intracellular signalling pathways. In one situation cellular antiviral responses can be misused by the virus of its own replication and at another point the same signalling pathway may even be turned into a pro-viral activity. When the impact of a given signalling pathway on viral growth is evaluated these bivalent functions of these pathways should be taken in consideration. Nevertheless, a signalling pathway that supports viral growth is an excellent target for antiviral therapy (Ludwig et al. 2003).
在过去几年中已有描述，流感病毒感染后会诱导多种细胞内信号通路。有实例和建议表明病毒复制周期如何导致细胞内信号通路的激活。病毒感染后多种信号通路被激活，作为对入侵病原体的一种警戒反应，可被视为宿主细胞的抗病毒反应。然而，也有研究表明，病毒能够抑制这些细胞反应以确保自身复制。此外，病毒还能够激活并滥用细胞信号通路以实现自身存活。核因子κB（NF-κB）信号通路就是这些情况的一个典型例子。由病毒介导的NF-κB信号通路的激活可被NS1蛋白部分阻断，以抑制强烈的抗病毒干扰素α/β反应。与此同时，病毒利用剩余的NF-κB活性进行与病毒相关的细胞凋亡及自身复制。这是病毒控制其复制的一种高效且经济的方式，无需特定的细胞反应病毒诱导剂。这表明，在流感病毒与细胞内信号通路的相互作用领域不存在“全或无”的反应。在一种情况下，细胞抗病毒反应可能被病毒用于自身复制，而在另一点上，相同的信号通路甚至可能转变为促病毒活性。在评估给定信号通路对病毒生长的影响时，应考虑这些通路的双重功能。然而，支持病毒生长的信号通路是抗病毒治疗的一个极佳靶点（路德维希等人，2003年）。
