Abstract

Innate immunity is the front line for antiviral immune responses and bridges adaptive immunity against viral infections. However, various viruses have evolved many strategies to evade host innate immunity. A typical virus is the porcine reproductive and respiratory syndrome virus (PRRSV), one of the most globally devastating viruses threatening the swine industry worldwide. PRRSV engages several strategies to evade the porcine innate immune responses. This review focus on the underlying mechanisms employed by PRRSV to evade pattern recognition receptors signaling pathways, type I interferon (IFN-α/β) receptor (IFNAR)-JAK-STAT signaling pathway, and interferon-stimulated genes. Deciphering the antiviral immune evasion mechanisms by PRRSV will enhance our understanding of PRRSV’s pathogenesis and help us to develop more effective methods to control and eliminate PRRSV.

Highlights

  • Since its discovery in the late 1980s, porcine reproductive and respiratory syndrome (PRRS) has become one of the most serious swine diseases in the world

  • PRRS virus (PRRSV) Types 1 and 2 were reclassified as two species belonging to the genus Porartevirus, PRRSV-1, and PRRSV-2, respectively, according to the current taxonomy (Adams et al, 2016)

  • A previous study shows that PRRSV infection inhibits IFNβ production primarily by interfering with the MAVS activation in the RIG-I signaling pathway (Luo et al, 2008)

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Summary

Introduction

Since its discovery in the late 1980s, porcine reproductive and respiratory syndrome (PRRS) has become one of the most serious swine diseases in the world. Porcine RIG-I, MDA5, and mitochondrial antiviral signaling protein (MAVS, known as IPS-1/VISA/Cardif) are important sensors/adaptors to produce type I IFN in the porcine innate immune system (Wang et al, 2008; Husser et al, 2011; Dong et al, 2013). RIG-I and MDA5 are well-conserved cytoplasmic PRRs that detect viral RNAs and interact with the downstream adaptor MAVS and activate the antiviral signaling pathway (Wu and Hur, 2015).

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