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

Bo Yang,Zixiang Zhu,Haixue Zheng,Dajun Zhang,Guowei Xu,Chaochao Sheng,Keshan Zhang,Xiangtao Liu,Jing Hou,Xiaohui Zhang,Sk Mohiuddin Choudhury,Dan Li

doi:10.3390/pathogens9090729

Bo Yang, Zixiang Zhu + Show 10 more

Open Access

https://doi.org/10.3390/pathogens9090729

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Journal: Pathogens	Publication Date: Sep 4, 2020
Citations: 12	License type: CC BY 4.0

Affiliation: Lanzhou Veterinary Research Institute

Abstract

Foot-and-mouth disease virus (FMDV) causes a highly contagious vesicular disease in cloven-hoofed livestock that results in severe consequences for international trade, posing a great economic threat to agriculture. The FMDV infection antagonizes the host immune responses via different signaling pathways to achieve immune escape. Strategies to escape the cell immune system are key to effective infection and pathogenesis. This review is focused on summarizing the recent advances to understand how the proteins encoded by FMDV antagonize the host innate and adaptive immune responses.

Highlights

Foot-and-mouth disease (FMD) is an acute and highly contagious disease affecting the cloven-hoofed animals, such as pigs and cattle
The Foot-and-mouth disease virus (FMDV) infection stimulates the expression of miR-1307, which indirectly induces the degradation of FMDV VP3 protein through the proteasome pathway and strengthens the host immune response to inhibit the replication of FMDV [62]
The infection level of FMDV decreased after the transient expression of 3AB protein. These findings suggested that 3A and 3AB play a crucial role in the replication of FMDV [110]

Summary

Introduction

Foot-and-mouth disease (FMD) is an acute and highly contagious disease affecting the cloven-hoofed animals, such as pigs and cattle. The mechanism of virus immune escape can be divided into three categories: (1) enable the virus to avoid the recognition of humoral immune response; (2) interfere with the function of cellular immune response; (3) interfere with the host’s immune response to the virus [10]. All these strategies would be exploited by the virus for replication and spreading to other hosts. New mechanisms and functions of FMDV proteins inhibiting innate immunity have been discovered. Multiple structural and non-structural proteins of FMDV escape the killing of the host immune system. The flank of ORF is a long 5’ untranslated region (5’-UTR) and a short 3’-UTR

Molecular

Molecular Mechanisms in FMDV Non-Structural Protein Immune Escape

Molecular Mechanisms for FMDV Untranslated Region in Immune Escape

Prospects and Future Directions

Conclusions