Foot-and-Mouth Disease Virus 3A Protein Causes Upregulation of Autophagy-Related Protein LRRC25 To Inhibit the G3BP1-Mediated RIG-Like Helicase-Signaling Pathway
Wenping Yang, Dan Li, Yi Ru, Juncui Bai, Jingjing Ren, Jing Zhang, Lulu Li, Xiangtao Liu, Haixue Zheng
Abstract
We show that foot-and-mouth disease virus (FMDV) 3A inhibits retinoic acid-inducible gene I (RIG-I)-like helicase signaling by degrading G3BP1 protein. Furthermore, FMDV 3A reduces G3BP1 by upregulating the expression of autophagy-related protein LRRC25. Additionally, other picornavirus 3A proteins, such as Seneca Valley virus (SVV) 3A, enterovirus 71 (EV71) 3A, and encephalomyocarditis virus (EMCV) 3A, also degrade G3BP1 by upregulating LRRC25 expression. This study will help us improve the design of current vaccines and aid the development of novel control strategies to combat FMD.
Topics & Concepts
BiologyPicornavirusHelicaseAutophagyDownregulation and upregulationVirologyVirusRIG-IFoot-and-mouth disease virusRNA Helicase AEnterovirus 71GeneEnterovirusRNAGeneticsApoptosisAnimal Disease Management and EpidemiologyViral Infections and Immunology ResearchViral Infections and Vectors