Fig. 1

Type I IFN signaling pathway and transcriptional changes of selected ISGs in the spinal cord of TMEV- compared to mock-infected SJL/J mice. Left side: Pattern recognition receptors (PKR, RIG-I-like helicases, Toll-like receptors) recognize viral proteins and RNA, which induce the activation of second messengers (IFN regulatory factors, NF-κB). These signal transducers translocate into the nucleus and induce the transcription of IFNα/β. Right side: These type I IFNs bind to the type I IFN receptor (IFNAR) to initiate signal transduction via the JAK-STAT pathway. This pathway activates specific transcription factors (ISGF3), which translocate into the nucleus, bind to IFN-stimulated response element (ISRE) of the DNA, and induce the transcription of abundant ISGs including ISG15, PKR, OAS, and Mx. Thermometer-like icons display significant fold changes (P ≤ 0.05) at four time points (1 = 14 dpi, 2 = 42 dpi, 3 = 98 dpi, 4 = 196 dpi). Legend: IFN interferon, ISG IFN-stimulated gene, ISG15 ISG of 15 kDa, ISGF3 ISG factor 3, JAK janus kinase, Mx myxovirus-resistance gene, NF-κB nuclear factor of kappa light polypeptide gene enhancer in B cells, OAS 2′, 5′-oligoadenylate-synthetase, PKR protein kinase R, RIG-I retinoic acid-inducible gene, STAT signal transducer and activator of transcription, TMEV Theiler’s murine encephalomyelitis virus