Fig. 3.

IFN response induced by viral infection. Virus or viral product recognition by TLR3 or RLRs leads to the activation of TLR3 or RLRs, which finally induce IFN production. The secreted IFN affects the cell through a paracrine or autocrine regulation and stimulates the expression of ISGs. An ISG, either OAS or PKR, activates RNase L via 2′, 5′-oligoadenylate synthetase or phosphorylation of eIF2, resulting in RNA degradation or translational suppression. The IFN response inhibits viral replication and damage to the cell. IFN, interferon; LGP2, laboratory of genetics and physiology 2; MDA5, melanoma differentiation-associated gene 5; TLR3, toll-like receptor 3; RLRs, retinoic acid-inducible gene I (RIG-I)-like receptors; ISGs, FN-stimulated genes; OAS, oligoadenylate synthetase; PKR, protein kinase R; eIF2-α, eukaryotic translation initiation factor 2α; IFNR, interferon receptor.