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. 2018 Jun 20;9:1379. doi: 10.3389/fimmu.2018.01379

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Copyright © 2018 Yong and Luo.

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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Viral RNA is recognized by RIG-I-like receptors (RLRs), RIG-I, or melanoma differentiation-associated protein 5 (MDA5). Activated RLRs interacts with mitochondria antiviral signaling protein (MAVS) adapter protein via CARD–CARD interactions. Activated MAVS then interacts with tumor necrosis factor receptor-associated factors 3 (TRAF3), tumor necrosis factor receptor-associated factors 6 (TRAF6), tumor necrosis factor receptor type-1-associated death domain (TRADD), receptor interacting serine/threonine-protein kinase 1 (RIP1), Fas-associated protein with death domain (FADD), and other signaling molecules. TRAF3 activates TANK binding kinase 1 (TBK1) and IκB kinase ε (IKKε), which phosphorylates interferon regulatory factors 3 and 7 (IRF3 and IRF7). The phosphorylated IRF3 and IRF7 dimerize and translocate into the nucleus to induce type 1 interferon response. On the other hand, MAVS interaction with receptor interacting serine/threonine-protein kinase 1, FADD, TRAF6, and TRADD. TRAF 6 ubiquitinate NF-kappa-B essential modulator (NEMO) which then activates IκB kinase and activates NF-κB. NF-κB transcription factor drives the expression of type 1 interferon and proinflammatory cytokines.