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. 2018 Mar 5;9:320. doi: 10.3389/fimmu.2018.00320

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Copyright © 2018 Chen, Liu, Goraya, Maarouf, Huang and Chen.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Schematic diagram for innate immune response against influenza A virus (IAV) infection. Intracellular detection of IAV infection by the host pathogen recognition receptors (PRRs) activates transcription factors nuclear factor kappa-light-chain-enhancer of activated B cells, interferon regulatory factor 3 (IRF3), and IRF7. The PRRs include retinoic acid-inducible gene-I protein, melanoma differentiation-associated gene 5, and toll-like receptors. Then these activated transcription factors trigger the expression of type I and type III interferons (IFNs). IFNs secreted by the infected cells interact with their receptors, which results in activation of Janus kinase-signal transducer and activator of transcription signaling pathway that governs the expression of various IFN-stimulated genes.