Abstract
The non-specific innate immunity can initiate host antiviral innate immune responses within minutes to hours after the invasion of pathogenic microorganisms. Therefore, the natural immune response is the first line of defense for the host to resist the invaders, including viruses, bacteria, fungi. Host pattern recognition receptors (PRRs) in the infected cells or bystander cells recognize pathogen-associated molecular patterns (PAMPs) of invading pathogens and initiate a series of signal cascades, resulting in the expression of type I interferons (IFN-I) and inflammatory cytokines to antagonize the infection of microorganisms. In contrast, the invading pathogens take a variety of mechanisms to inhibit the induction of IFN-I production from avoiding being cleared. Pseudorabies virus (PRV) belongs to the family Herpesviridae, subfamily Alphaherpesvirinae, genus Varicellovirus. PRV is the causative agent of Aujeszky’s disease (AD, pseudorabies). Although the natural host of PRV is swine, it can infect a wide variety of mammals, such as cattle, sheep, cats, and dogs. The disease is usually fatal to these hosts. PRV mainly infects the peripheral nervous system (PNS) in swine. For other species, PRV mainly invades the PNS first and then progresses to the central nervous system (CNS), which leads to acute death of the host with serious clinical and neurological symptoms. In recent years, new PRV variant strains have appeared in some areas, and sporadic cases of PRV infection in humans have also been reported, suggesting that PRV is still an important emerging and re-emerging infectious disease. This review summarizes the strategies of PRV evading host innate immunity and new targets for inhibition of PRV replication, which will provide more information for the development of effective inactivated vaccines and drugs for PRV.
Highlights
Virus infection induces host innate immune responses, which play an important and decisive role in determining the outcome of the infected host, inducing acute infection death or establishing persistent infection in mammals
For RNA virus, viral RNA is often recognized by a variety of pattern recognition receptors (PRRs), including endosomal Toll-like receptor 3 (TLR3), cytosolic retinoic acid-inducible gene I (RIG-I), melanoma differentiation-associated gene 5 (MDA5), and
PRRs recruit a series of important signal transduction molecules, such as myeloid differentiation primary response gene 88 (MyD88), mitochondrial antiviral-signaling protein (MAVS), intracellular stimulator of IFN genes (STING). These proteins transfer the different signals to the downstream molecules in different signaling pathways, which eventually lead to activation and translocation of several transcription factors, including NF-κB, interferon regulatory factor 3 (IRF3), and IRF7 into the nucleus to induce the expression of IFN-I and proinflammatory cytokines [10–12]
Summary
Guangqiang Ye 1 , Hongyang Liu 1 , Qiongqiong Zhou 1 , Xiaohong Liu 1 , Li Huang 1,2 and Changjiang Weng 1,2, *. Heilongjiang Provincial Key Laboratory of Veterinary Immunology, Harbin 150069, China
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