Molecular Mechanisms of Immune Escape for Foot-and-Mouth Disease Virus

Figures

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  Figure 1. Schematic of the genome and polypeptide processing of FMDV [3,9]. The FMDV genome contains an ORF of about 7 kbp, indicated by the shaded rectangle. Each region within the ORF rectangle represents a single protein. The flank of ORF is a long 5′ untranslated region (5′-UTR) and a short 3′-UTR. 3B covalently binds to the 5′-end.

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  Figure 2. Known functions of FMDV structural proteins on immune escape. Red or yellow arrow: activation of downstream protein. Red or yellow line with vertical stub: inhibition of downstream proteins. The capsid protein of FMDV mainly targets IFN signal pathway, NF-κB pathway, JAK-STAT pathway, MAPK pathway, autophagy-related pathway and host transcription-related protein. FMDV VP0 and VP3 reduce the expression of junction protein VISA at the transcriptional or protein level. FMDV VP0 and VP1 can directly or indirectly target IRF3 to inhibit interferon production. VP3 proteins inhibit JAK-STAT signaling pathway, thus inhibiting ISGs production. FMDV protein VP2 can promote virus replication by regulating autophagy. PCBP2: poly (rC) binding protein 2; NME1: nucleoside diphosphate kinase 1; HSPB1: heat shock protein family B [small] member 1; Sorcin: soluble resistance-related calcium binding protein; TPL2: tumor progression locus 2; RPSA: ribosomal protein SA; JAK1: janus kinase 1.

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  Figure 3. Known functions of FMDV non-structural proteins on immune escape. Red or yellow arrow: activation of downstream protein. Red or yellow line with vertical stub: inhibition of downstream proteins. As shown in the figure. FMDV structural proteins mainly targets IFN signal pathway, NF-κB pathway, JAK-STAT pathway, MAPK pathway, autophagy-related pathway and host transcription-related protein. FMDV (Lpro, 2B, 3A, 3B, 3C) can directly or indirectly act on retinoic acid-induced gene I-like receptor (RLR) to inhibit innate immunity. FMDV 3A and 3B reduce the expression of junction protein VISA at the transcriptional or protein level. Lpro, 2B and 3A can directly or indirectly target IRF3 to inhibit interferon production. 3C proteins inhibit JAK-STAT signaling pathway, thus inhibiting ISGs production. Lpro and 3C inhibit the synthesis of antiviral molecules by cutting related factors of host transcription and translation. Lpro protein can not only induce apoptosis, but also inhibit host cell apoptosis and promote virus replication, which is achieved by blocking the translation of α-IFN and inhibiting PKR synthesis. 2C can promote virus replication by regulating autophagy. eIF4G:…