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Interplay between influenza A virus and the innate immune signaling
Authors:Christina Ehrhardt  Roman Seyer  Eike R Hrincius  Thorsten Eierhoff  Thorsten Wolff  Stephan Ludwig
Institution:1. Institute of Molecular Virology (IMV), Center for Molecular Biology of Inflammation (ZMBE), Westfaelische-Wilhelms-University, Von Esmarch-Str. 56, D-48149 Muenster, Germany;2. Robert Koch Institute, P15, Nordufer 20, D-13353 Berlin, Germany;1. Biomedical Sciences Research Complex, University of St Andrews, North Haugh, St Andrews, Fife KY16 9ST, UK;2. Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford OX1 3RE, UK;1. Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Sciences, No. 518, Ziyue Road, Shanghai 200241, PR China;2. Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, No. 1, Xujiaping Road, Lanzhou 730046, PR China;1. Department of Medicine, Section of Rheumatology, The Knapp Center for Lupus and Immunology Research, The University of Chicago, Chicago, IL 60637, USA;2. Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA;3. Committee on Immunology, The University of Chicago, Chicago, IL 60637, USA
Abstract:Pathogens such as influenza A viruses (IAV) have to overcome a number of barriers defined and maintained by the host, to successfully establish an infection. One of the initial barriers is collectively characterized as the innate immune system. This is a broad anti-pathogen defense program that ranges from the action of natural killer cells to the induction of an antiviral cytokine response. In this article we will focus on new developments and discoveries concerning the interaction of IAV with the cellular innate immune signaling. We discuss new mechanisms of interference of IAV with the pathogen recognition receptor RIG-I and the type I IFN antagonist NS1 in the background of already known and established concepts. Further we summarize progress related to recently identified IFN induced proteins and the role of RNA interference in the context of IAV infection.
Keywords:
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