Explore the vast range of titles available.

Porcine epidemic diarrhea virus (PEDV) has been endemic in most parts of the world since its emergence in the 1970s. It infects the small intestine and intestinal villous cells, spreads rapidly, and causes infectious intestinal disease characterized by vomiting, diarrhea, and dehydration, leading to high mortality in newborn piglets and causing massive economic losses to the pig industry. The entry of PEDV into cells is mediated by the binding of its spike protein (S protein) to a host cell receptor. Here, we review the structure of PEDV, its strains, and the structure and function of the S protein shared by coronaviruses, and summarize the progress of research on possible host cell receptors since the discovery of PEDV.

Porcine epidemic diarrhea virus (PEDV), a member of the Alpha-coronavirus genus in the Coronaviridae family, induces acute diarrhea, vomiting, and dehydration in neonatal piglets. This study aimed to investigate the genetic dependencies of PEDV and identify potential therapeutic targets by using a single-guide RNA (sgRNA) lentiviral library to screen host factors required for PEDV infection. Protein kinase C θ (PKCθ), a calcium-independent member of the PKC family localized in the cell membrane, was found to be a crucial host factor in PEDV infection. The investigation of PEDV infection was limited in Vero and porcine epithelial cell-jejunum 2 (IPEC-J2) due to defective interferon production in Vero and the poor replication of PEDV in IPEC-J2. Therefore, identifying suitable cells for PEDV investigation is crucial. The findings of this study reveal that human embryonic kidney (HEK) 293T and L929 cells, but not Vero and IPEC-J2 cells, were suitable for investigating PEDV infection. PKCθ played a significant role in endocytosis and the replication of PEDV, and PEDV regulated the expression and phosphorylation of PKCθ. Apoptosis was found to be involved in PEDV replication, as the virus activated the PKCθ-B-cell lymphoma 2 (BCL-2) ovarian killer (BOK) axis in HEK293T and L929 cells to increase viral endocytosis and replication via mitochondrial apoptosis. This study demonstrated the suitability of HEK293T and L929 cells for investigating PEDV infection and identified PKCθ as a host factor essential for PEDV infection. These findings provide valuable insights for the development of strategies and drug targets for PEDV infection.

Background/Objectives: Porcine epidemic diarrhea (PED) is a highly contagious enteric disease caused by porcine epidemic diarrhea virus (PEDV) and is associated with severe clinical signs and high mortality in neonatal piglets. Vaccination is an important strategy for PED control through the induction of humoral immunity. This study aimed to compare immune responses induced by inactivated and live-attenuated PEDV vaccines and to evaluate a heterologous prime-boost vaccination strategy in PEDV-naïve replacement gilts. Methods: Twenty-four PEDV-naïve replacement gilts were randomly assigned to four groups: unvaccinated control, inactivated vaccine administered twice (K/K), live-attenuated vaccine administered twice (L/L), and live-attenuated priming followed by an inactivated booster (L/K). Pigs received two intramuscular vaccinations at 16 weeks of age and two weeks later. Serum samples collected up to 42 days post-vaccination were analyzed for PEDV-specific IgG and IgA antibodies by ELISA, and serum-neutralizing antibody titers were determined using a serum neutralization test. Results: The L/K regimen induced the highest PEDV-specific IgG responses, with peak levels at day 28 post-vaccination that were significantly higher than those in the K/K and control groups. Serum-neutralizing antibody titers were significantly higher in the L/K and L/L groups than in the K/K and control groups. Serum IgA responses were low and transient across all vaccination groups. Conclusions: A heterologous prime-boost vaccination strategy using a live-attenuated PEDV vaccine followed by an inactivated booster induces strong systemic humoral immune responses in replacement gilts and represents a promising approach for PEDV vaccination programs.

Porcine viral diarrhea diseases affect the swine industry, resulting in significant economic losses. Porcine epidemic diarrhea virus (PEDV) genotypes G1 and G2, and groups A and C of the porcine rotavirus, are major etiological agents of severe gastroenteritis and profuse diarrhea, particularly among piglets, with mortality rates of up to 100%. Based on the high prevalence rate and frequent co-infection of PEDV, RVA, and RVC, close monitoring is necessary to avoid greater economic losses. We have developed a multiplex TaqMan probe-based real-time PCR for the rapid simultaneous detection and differentiation of PEDV subtypes G1 and G2, RVA, and RVC. This test is highly sensitive, as the detection limits were 20 and 100 copies/μL for the G1 and G2 subtypes of PEDV, respectively, and 50 copies/μL for RVA and RVC, respectively. Eighty-eight swine clinical samples were used to evaluate this new test. The results were 100% in concordance with the standard methods. Since reassortment between porcine and human rotaviruses has been reported, this multiplex test not only provides a basis for the management of swine diarrheal viruses, but also has the potential to impact public health as well.

Porcine epidemic diarrhea virus (PEDV) continues to harm the global swine industry. It is important to develop a highly effective vaccine to control PEDV infection. Here, we report a PEDV spike (S) mRNA vaccine that primes a potent antibody response and antigen-specific T-cell responses in immunized piglets. Active and passive immunization can protect piglets against PED following the virus challenge. This study highlights the efficiency of the PEDV-S mRNA vaccine and represents a viable approach for developing an efficient PEDV vaccine.

Porcine epidemic diarrhea virus (PEDV), being highly virulent and contagious in piglets, has caused significant damage to the pork industries of many countries worldwide. There are no commercial drugs targeting coronaviruses (CoVs), and few studies on anti-PEDV inhibitors. The coronavirus 3C-like protease (3CLpro) has a conserved structure and catalytic mechanism and plays a key role during viral polyprotein processing, thus serving as an appealing antiviral drug target. Here, we report the anti-PEDV effect of the broad-spectrum inhibitor GC376 (targeting 3Cpro or 3CLpro of viruses in the picornavirus-like supercluster). GC376 was highly effective against the PEDV 3CLpro and exerted similar inhibitory effects on two PEDV strains. Furthermore, the structure of the PEDV 3CLpro in complex with GC376 was determined at 1.65 Å. We elucidated structural details and analyzed the differences between GC376 binding with the PEDV 3CLpro and GC376 binding with the transmissible gastroenteritis virus (TGEV) 3CLpro. Finally, we explored the substrate specificity of PEDV 3CLpro at the P2 site and analyzed the effects of Leu group modification in GC376 on inhibiting PEDV infection. This study helps us to understand better the PEDV 3CLpro substrate specificity, providing information on the optimization of GC376 for development as an antiviral therapeutic against coronaviruses.

The porcine epidemic diarrhea virus (PEDV) is a member of the coronavirus family, causing deadly watery diarrhea in newborn piglets. The global pandemic of PEDV, with significant morbidity and mortality, poses a huge threat to the swine industry. The currently developed vaccines and drugs are only effective against the classic GI strains that were prevalent before 2010, while there is no effective control against the GII variant strains that are currently a global pandemic. In this review, we summarize the latest progress in the biology of PEDV, including its transmission and origin, structure and function, evolution, and virus–host interaction, in an attempt to find the potential virulence factors influencing PEDV pathogenesis. We conclude with the mechanism by which PEDV components antagonize the immune responses of the virus, and the role of host factors in virus infection. Essentially, this review serves as a valuable reference for the development of attenuated virus vaccines and the potential of host factors as antiviral targets for the prevention and control of PEDV infection.

•Coated PEDV-loaded microspheres were developed by centrifugal granulation-fluidized bed coating.•Coated PEDV-loaded microspheres could protect PEDV antigens against the complex gastrointestinal environment in vitro and in vivo.•Oral vaccination with coated PEDV-loaded microspherescould induce higher levels of PEDV-specific antibodies in weaned piglets than the orally delivered PEDV only group. Porcine epidemic diarrhea virus (PEDV) infects pigs of all ages by invading villous epithelial cells of the small intestine causing severe diarrhea with high mortality rate in suckling piglets. Mucosal immunity is believed to play an important role in PEDV control and mucosal delivery of vaccines induces mucosal immunity more efficiently than parenteral vaccination. In this study, coated PEDV-loaded microspheres with the size range of 700–900 μm in diameter were developed by centrifugal granulation-fluidized bed coating and demonstrated as an effective oral delivery system to protect PEDV antigens against the complex gastrointestinal environment by detecting the live virus particles in microspheres after the simulated gastric fluid treatment and the PEDV RNA in fecal swabs collected from all weaned piglets (100%) orally inoculated with coated PEDV-loaded microspheres. Weaned piglets orally immunized with coated PEDV-loaded microspheres developed higher levels of PEDV-specific antibodies (IgG and IgA) in their sera and saliva than those negative control groups (p < 0.001 or p < 0.01). Furthermore, neutralization assays demonstrated that serum antibodies in coated PEDV-loaded microspheres groups could significantly inhibit virus infection in Vero cells, compared to PEDV only group (p < 0.05). Overall, our results indicate that the coated PEDV-loaded microspheres might serve as an effective way to induce PEDV-specific mucosal immunity in pigs against PEDV.

The enteric disease of swine recognized in the early 1970s in Europe was initially described as “epidemic viral diarrhea” and is now termed “porcine epidemic diarrhea (PED)”. The coronavirus referred to as PED virus (PEDV) was determined to be the etiologic agent of this disease in the late 1970s. Since then the disease has been reported in Europe and Asia, but the most severe outbreaks have occurred predominantly in Asian swine-producing countries. Most recently, PED first emerged in early 2013 in the United States that caused high morbidity and mortality associated with PED, remarkably affecting US pig production, and spread further to Canada and Mexico. Soon thereafter, large-scale PED epidemics recurred through the pork industry in South Korea, Japan, and Taiwan. These recent outbreaks and global re-emergence of PED require urgent attention and deeper understanding of PEDV biology and pathogenic mechanisms. This paper highlights the current knowledge of molecular epidemiology, diagnosis, and pathogenesis of PEDV, as well as prevention and control measures against PEDV infection. More information about the virus and the disease is still necessary for the development of effective vaccines and control strategies. It is hoped that this review will stimulate further basic and applied studies and encourage collaboration among producers, researchers, and swine veterinarians to provide answers that improve our understanding of PEDV and PED in an effort to eliminate this economically significant viral disease, which emerged or re-emerged worldwide.