Interplay between influenza A virus and the innate immune signaling.
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.
Institute of Molecular Virology (IMV), Center for Molecular Biology of Inflammation (ZMBE), Westfaelische-Wilhelms-University, Muenster, Germany.
Christina
C
Ehrhardt
Roman
R
Seyer
Eike R
ER
Hrincius
Thorsten
T
Eierhoff
Thorsten
T
Wolff
Stephan
S
Ludwig
D000818:Animals; D000071457:DEAD Box Protein 58; D053487:DEAD-box RNA Helicases / Q000037:antagonists & inhibitors; D054884:Host-Pathogen Interactions; D006801:Humans; D007113:Immunity, Innate; D009980:Influenza A virus / Q000276:immunology*; D007370:Interferon Type I / Q000037:antagonists & inhibitors; D011971:Receptors, Immunologic; D015398:Signal Transduction; D017361:Viral Nonstructural Proteins / Q000276:immunology; D037521:Virulence Factors / Q000276:immunology
C085820:INS1 protein, influenza virus; D007370:Interferon Type I; D011971:Receptors, Immunologic; D017361:Viral Nonstructural Proteins; D037521:Virulence Factors; C452820:RIGI protein, human; D000071457:DEAD Box Protein 58; D053487:DEAD-box RNA Helicases