Figure 1.

Antiviral defense of IFN. (a) Viral RNA (vRNA) can be recognized by pathogen pattern receptors (PPR) on the cell surface and retinoic acid-like receptors (RLR) in the cytosol. The vRNA sensing by PPR can be initiated by toll-like receptors (TLR)-3, -7, and -8, which then activates gene transcription factors, i.e., interferon regulatory factors (IRF)-3 and -7. IRF-3 and -7 are then translocated into the cell nucleus to express interferon (IFN)-β and interferon-α, respectively. The cytosolic viral dsRNA, on the other hand, is recognized by retinoic-like receptors (RLR) such as retinoic acid-inducible gene-1 (RIG-I) and melanoma differentiation-associated protein 5 (MDA-5). The RLR/vRNA complex subsequently binds to the mitochondrial-antiviral signaling (MAVS) protein located on the mitochondrial outer membrane. Upon the activation of MAVS, IRF-3 is phosphorylated via TANK-binding kinase (TBK)-1 to enhance the expression of IFN-β. (b) The antiviral cascades of IFN α/β demand the activation of Janus kinase/tyrosine kinase/signal transducer and activator of transcription (JAK/TYK/STAT) signaling. Activating the JAK/TYK/STAT transcription signaling pathway results in the expression of antiviral proteins, oligoadenylate synthetase (OAS), and protein kinase R (PKR), which are responsible for viral RNA degradation and inhibition of viral protein synthesis, respectively.