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. 2018 Aug 13;9:1862. doi: 10.3389/fmicb.2018.01862

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Copyright © 2018 Ma, Ma, Chang, Ma, Li, Wang, Ma and Cao.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Evasion of antiviral response of type I IFN mediated by FMDV. FMDV Lpro can cleave the p65 subunit of NF-κB and inhibit IRF3/7, which promote the interferon-stimulated response element (ISRE). FMDV 3C^pro blocks the translocation of STAT1-STAT2 complex to the nucleus and suppresses the ISKE promoter. Recombinant VP1 can disrupt the formation of the canonical IKK complex to block NF-κB activity. VP3 can disrupt the assembly of the Jak1/STAT1 complex and inhibit IRF3 phosphorylation and dimerization. FMDV 2B can bind to RIG-I or LGP2 to impair related signal transduction and enhance viral replication. FMDV 3A protein can disrupt the transcriptional levels involved in RIG-I, MDA5, and MAVS and block the interaction between RIG-I/MDA5 and MAVS via its N-terminal region.