[Mechanisms underlying interferon-mediated host innate immunity during influenza A virus infection].
Influenza A virus can create acute respiratory infection in humans and animals throughout the world, and it is still one of the major causes of morbidity and mortality in humans worldwide. Numerous studies have shown that influenza A virus infection induces rapidly host innate immune response. Influenza A virus triggers the activation of signaling pathways that are dependent on host pattern recognition receptors (PRRs) including toll like receptors (TLRs) and RIG-I like receptors (RLRs). Using a variety of regulatory mechanisms, these signaling pathways activate downstream transcript factors that control expression of various interferons and cytokines, such as type I and type III interferons. Thus, these interferons stimulate the transcript of relevant interferon-stimulated genes (ISGs) and expression of the antiviral proteins, which are critical components of host innate immunity. In this review, we will highlight the mechanisms by which influenza A virus infection induces the interferon-mediated host innate immunity.
Chao
C
Chen
Xiaojuan
X
Chi
Qingling
Q
Bai
Jilong
J
Chen
D016207:Cytokines / Q000276:immunology; D000071457:DEAD Box Protein 58; D053487:DEAD-box RNA Helicases / Q000276:immunology; D006801:Humans; D007113:Immunity, Innate; D009980:Influenza A virus; D007251:Influenza, Human / Q000276:immunology*; D007372:Interferons / Q000276:immunology*; D011971:Receptors, Immunologic; D051192:Receptors, Pattern Recognition / Q000276:immunology; D015398:Signal Transduction; D051193:Toll-Like Receptors / Q000276:immunology
D016207:Cytokines; D011971:Receptors, Immunologic; D051192:Receptors, Pattern Recognition; D051193:Toll-Like Receptors; D007372:Interferons; C452820:RIGI protein, human; D000071457:DEAD Box Protein 58; D053487:DEAD-box RNA Helicases