Abstract
Porcine epidemic diarrhea virus (PEDV), a swine enteropathogenic coronavirus (CoV), is the causative agent of porcine epidemic diarrhea (PED). PED causes lethal watery diarrhea in piglets, which has led to substantial economic losses in many countries and is a great threat to the global swine industry. Interferons (IFNs) are major cytokines involved in host innate immune defense, which induce the expression of a broad range of antiviral effectors that help host to control and antagonize viral infections. PEDV infection does not elicit a robust IFN response, and some of the mechanisms used by the virus to counteract the host innate immune response have been unraveled. PEDV evades the host innate immune response by two main strategies including: 1) encoding IFN antagonists to disrupt innate immune pathway, and 2) hiding its viral RNA to avoid the exposure of viral RNA to immune sensors. This review highlights the immune evasion mechanisms employed by PEDV, which provides insights for the better understanding of PEDV-host interactions and developing effective vaccines and antivirals against CoVs.
Highlights
Porcine epidemic diarrhea virus (PEDV) is the etiological agent of porcine epidemic diarrhea (PED)that causes an acute and highly contagious enteric disease of swine characterized by vomiting, diarrhea, dehydration, and anorexia in pigs of all ages, especially resulting in severe diarrhea and high mortality rate in piglets
The activation of type I IFN responses is composed of three stages: (1) recognition of pathogen-associated molecular pattern (PAMP) by PRRs; (2) secretion of type I IFNs through paracrine or autocrine pathways; and (3) expression of numerous antiviral IFN-stimulated genes (ISGs) which bring the host into the antiviral state [136]
The role of nsp ExoN activity of PEDV in counteracting host antiviral response should be investigated to uncover more functions of PEDV nsps. These data suggest that PEDV has evolved multiple evasive mechanisms to circumvent viral RNA recognition or prevent RNA degradation to establish a successful infection in the host
Summary
Porcine epidemic diarrhea virus (PEDV) is the etiological agent of porcine epidemic diarrhea (PED). Vaccination used to be the main strategy to prevent and control the rate of PEDV infection [14], the current available PEDV vaccines cannot provide complete protection for the pigs affected by the highly pathogenic strains. The highly pathogenic variant strains of PEDV were identified in 2010 and caused a high morbidity of up to 100% in piglets, and since these strains become dominant, leading to most of the acute outbreaks of PED worldwide [1,7,8]. PEDV has evolved different strategies to delicately manipulate and damage the host innate immune system for their multiplication Clarification of these mechanisms is critical for understanding the host range, tropisms, pathogenesis, and for developing effective vaccines and antiviral drugs to curb the spread of PEDV in pigs. We provide an overview of different mechanisms used by PEDV to evade host innate immune responses
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