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. 2016 Nov 16;8(11):308. doi: 10.3390/v8110308

Figure 2.

Figure 2

A detailed overview of host factors involved in MeV-stimulated interferon (IFN) induction and signaling. The C and V proteins inhibit the activation of the viral RNA sensors retinoic-acid inducible gene I (RIG-I), melanoma differentiation-associated protein 5 (MDA5) and RIG-I-like receptor 2 (LGP2) and the following IFN responses. Furthermore, V protein inhibits the activation and function of interferon regulatory transcription factor 3 (IRF-3) and IRF-7 via interaction with them. The P, V, and C proteins bind subunits of nuclear factor-kappa B (NF-κB) and repress the production of IFN-β and cytokine. In addition, the interaction between P protein and the negative regulator A20 also leads to the repression of NF-κB. In addition, sphingosine kinase 1 (SK1) interacts with TNF receptor-associated factor 2 (TRAF2) and enhances tumor necrosis factor (TNF)-induced activation of NF-κB signaling. In the nucleus, C protein represses IFN-β transcription without inhibiting the activation of IRF-3. On the contrary, N protein positively activates the IRF-3 and IFN-β production. The interferon inducible protein ADAR1 negatively regulates the activation of protein kinase regulated by RNA (PKR) and the IRF-3, suppressing MeV-mediated IFN-β production. To interfere with the IFN signaling, C protein blocks the dimerization of phosphorylated signal transducer and activator of transcription 1 (STAT-1). P and V protein inhibit the phosphorylation and nuclear translocation of STAT-1. In addition, N protein can prevent the migration of STAT-1 and STAT-2 into nucleus. The IFN signaling triggers the expression of many IFN-inducible proteins. The arrows indicate the activation of IFN responses while the T-ended arrows indicate the repression by MeV. JAK-1, Janus kinase 1; TYK-2, tyrosine kinase 2; ISG IFN-stimulated gene; IRF, interferon regulatory factor; IKK, IκB kinase; TLR, Toll-like receptor; ADAR1, adenosine deaminase acting on RNA 1; MAVS, mitochondrial antiviral-signaling protein; OAS, 2′-5′-oligoadenylate synthetase; IRAK, interleukin-1 receptor-associated kinase 1.