Fig. 2.

Overview of established and potential pathways targeted by SOCS proteins in a cell infected by HSV-1 and/or EBV. After HSV-1 infection and the stimulation of several pathogen recognition receptors (MDA5, RIG-1, TLR1/TLR2, TLR3, TLR7, TLR9), IFNβ is transcriptionally activated following the stimulation of various signalling pathways. SOCS proteins can act at different levels (inhibition of the JAK activity, competition with recruited STAT proteins for shared phosphotyrosine residues, phosphorylation of receptor tyrosine residues, ubiquitination and degradation of bound protein components) in the cell as indicated by stop signs. Question marks (?) indicate pathways that are possibly targeted by SOCS to modulate the anti-viral immune response. DDX3, Dead box protein 3; dsRNA, double stranded ribonucleic acid; EBV, Epstein-Barr Virus; HSV-1, Herpes Simplex Virus type 1; IFN, interferon; IKKα, I kappa-B kinase-alpha; IKKβ, I kappa-B kinase-beta; IKKi, kinase I kappa B kinase i; iNOS, inducible nitric oxide synthase; IRE, interferon response element; IRAK, IL1-Receptor-associated kinase; IRF, IFN-regulatory factor; JAK, janus kinase; MAVS, mitochondrial antiviral signalling protein; MDA5, melanoma differentiation-associated gene 5; MYD88, myeloid differentiation primary-response protein 88; NF-kβ, Nuclear factor kappa-B; P, phosphorylated tyrosine; p50, p50 subunit of NF-κB; TBK1, TANK-binding kinase 1; TRIF, TIR-containing adaptator inducing interferon-β;TLR, toll like receptor; TRAF, Tumor necrosis factor receptor (TNFR)-associated factor; RIG-1, Retinoic acid-inducible gene I; STAT, signal transduction and activators of transcription.