Abstract
Porcine epidemic diarrhea virus (PEDV) infection causes watery diarrhea, dehydration, and high mortality in neonatal pigs, due to its clinical pathogenesis of the intestinal mucosal barrier dysfunction. The host's innate immune system is the first line of defence upon virus invasion of the small intestinal epithelial cells. In turn, the virus has evolved to modulate the host's innate immunity during infection, resulting in pathogen virulence, survival, and the establishment of successful infection. In this review, we gather current knowledge concerning the interplay between PEDV and components of host innate immunity, focusing on the role of cytokines and interferons in intestinal antiviral innate immunity, and the mechanisms underlying the immune evasion strategies of PEDV invasion. Finally, we provide some perspectives on the potential prevention and treatment for PEDV infection.
Highlights
Porcine epidemic diarrhea (PED) is an infectious and highly contagious viral disease in pigs characterized by anorexia, vomiting, watery diarrhea, dehydration, and body weight loss and has a high mortality, especially in neonatal pigs. e etiological agent of PED is porcine epidemic diarrhea virus (PEDV), which targets the digestive tract of pigs
Previous in vitro and in vivo research demonstrated that TLR2, TLR3, TLR4, TLR7, and TLR9 were involved in PEDV-induced NF-κB activation in porcine intestinal epithelial cells (IECs), suggesting that the virus can exploit its surface glycoprotein and intranuclear nucleic acids to trigger the innate immunity [29, 30]
Studies have shown that dietary supplementation of 200 and 500 IU vitamin D can mitigate the damage of porcine rotavirus in pigs and significantly increase the expression of retinoic acid-inducible gene (RIG)-I and IFN-β promoter stimulator-1 (IPS-1) and the mRNA levels of IFN-β and ISG15, indicating that supplementation of vitamin D activates the RIG-I signalling pathway, inducing the expression of IFNs and antiviral factors to alleviate the adverse impact of the virus [71]
Summary
Porcine epidemic diarrhea (PED) is an infectious and highly contagious viral disease in pigs characterized by anorexia, vomiting, watery diarrhea, dehydration, and body weight loss and has a high mortality, especially in neonatal pigs. e etiological agent of PED is porcine epidemic diarrhea virus (PEDV), which targets the digestive tract of pigs. After PEDV invades host cells, its genomic nucleic acid, doublestranded RNA (dsRNA), and protein produced during replication mediate two predominant signalling pathways (the RLR signalling pathway and TLR signalling pathway) in the natural immune response to exhibit congenital antiviral function. Previous in vitro and in vivo research demonstrated that TLR2, TLR3, TLR4, TLR7, and TLR9 were involved in PEDV-induced NF-κB activation in porcine intestinal epithelial cells (IECs), suggesting that the virus can exploit its surface glycoprotein and intranuclear nucleic acids to trigger the innate immunity [29, 30].
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