Abstract
Porcine diarrhea disease in newborn and suckling piglets due to infection with porcine epidemic diarrhea virus (PEDV) is a leading cause of economic loss in the pig industry globally. In this study, we investigated the molecular mechanism of the host innate immune response to PEDV infection. The expression dynamics of antiviral genes (e.g., RIG-1, PKR, OAS1, Mx1, and Mx2) and inflammatory cytokines (e.g., IFN-α, IFN-β, TNF-α, IL-6, IL-8, and IL-12) in porcine small intestinal epithelial (IPEC-J2) cells were analyzed following PEDV stimulation. The results showed that the expression of antiviral genes (e.g., PKR, OAS1, and Mx2) and inflammatory cytokines (e.g., IFN-α and TNF-α) were significantly reduced within 0–4 h post-infection (P < 0.05). However, all antiviral genes and inflammatory cytokines were up-regulated from 12 to 24 h (P < 0.05), and cytopathic changes were observed during this time. The expression of RIG-1, PKR, OAS1, Mx1, and Mx2 were significantly and positively correlated to each other during the entire infection (P < 0.01). The results suggested that the RIG-1, PKR, OAS1, Mx1, and Mx2 genes may play an important role in PEDV infection in piglets. Initially, PEDV displayed cellular invasion by inhibiting IFN-α transcription and interfering with the antiviral function of PKR, OAS1, and Mx2, ultimately induced an intense inflammatory response. The relationship between antiviral genes and inflammatory cytokines with PEDV infection at the cellular level provides a reference for studying the mechanism of resistance to PEDV infection in piglets.
Highlights
Porcine epidemic diarrhea (PED) is a swine infectious disease characterized by levels of susceptibility, high incidence, and fatality
The relationship between porcine epidemic diarrhea virus (PEDV) infection and host natural immunity has become an issue of keen interest throughout the world
PEDV is positive sense single-stranded RNA virus coated with a capsid for which the pathogenesis is associated with the binding of the S1 subunit region of the virus-encoded S protein to the receptor gene (APN) expressed on porcine small intestinal epithelial cells [15]
Summary
Porcine epidemic diarrhea (PED) is a swine infectious disease characterized by levels of susceptibility, high incidence, and fatality. PED was first discovered in the United Kingdom in 1971 and successively erupted in Europe, Asia, America, and other regions within the 40 years [1,2,3,4,5]. PED has become an important epidemic that restricts the development of the pig industry, causing serious economic losses. Porcine epidemic diarrhea virus (PEDV) is the causative agent of PED, which was discovered and termed, CV777, in 1978 [6]. PEDV invades the digestive system of pigs through the nose and mouth, targeting, and residing in the porcine small intestinal. PEDV subsequently destroys the mucosal immune barrier of the small intestine, causing watery diarrhea, dehydration, and vomiting in piglets. The control measures for PED mainly include the vaccination of pregnant sows; neither attenuated nor inactivated vaccines have been significantly effective in practice [8, 9]
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