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Porcine Epidemic Diarrhea Virus (PEDV) is a member of the Coronavirus family and genus, and is a single stranded RNA virus with a high degree of variation. PEDV is intolerant to high temperatures and can effectively kill the virus at temperatures above 60 ℃. Conventional disinfectants such as ether, chloroform, and other fat soluble solvents are effective. This virus is highly susceptible to co infection with other diarrhea causing viruses and bacteria, and the death of infected pigs is even more severe. PEDV has only one serotype, but the virus has high variability and exists in multiple different genotypes. At present, there are two main genotypes of PEDV prevalent worldwide, namely G Ⅰ (classical strain) and G Ⅱ (mutant strain). The Anti-Porcine Epidemic Diarrhea Virus Monoclonal Antibody serves as a critical reagent in immunodiagnostic assays, enabling highly specific detection and characterization of viral antigens in research and outbreak investigations.
PEDV prefers to infect and replicate in the swine intestinal tract, including the villous epithelial cells of the small intestine and jejunum, and the surface epithelial cells of the caecum and colon, of which the jejunum and ileum are the main sites of infection. Infection with PEDV promotes fusion between cells, leading to continuous necrosis of cells, resulting in severe diarrhea and even death in piglets. At the same time, PEDV is sensitive to the porcine liver, resulting in abnormal cholesterol metabolism genes, and disrupting the metabolic homeostasis of cholesterol. A comprehensive understanding of the infection mechanism by which PEDV invades host cells and achieves replication has important implications for the prevention and control of viral infection. Firstly, PEDV relies on serine proteolysis and low pH to enter cells through endocytosis, which is the entry mechanism by which PEDV infects the host. Secondly, PEDV mainly utilizes viral components to evade the host's innate immune responses during host infection. It is well known that after the virus invades the host cells, interferon (IFN) plays an important role as a key signaling molecule to block virus infection, especially type I IFNs, which clear the virus by activating various immune cells and costimulatory molecules.
Figure 1. Schematic diagram of PEDV evading the host innate-immune signaling pathway. (Zhang, Yuanzhu,et al, 2022)
| Host Factors | Function | Role in VIRAL Infection |
| Neu5Ac | As a cell surface glycoprotein; immune regulation and recognition; viral interactions | As a sugar coreceptor for PEDV entry cells |
| Occludin | A tight junction protein; signal transduction; innate immune regulation | As a PEDV entry cofactor |
| NPM1 | Ribosome assembly and chromatin remodeling; nuclear export; cell growth regulation | Interacts with N protein to promote PEDV growth |
| HSP70 | Protein folding; participates in cellular processes; promotes viral replication. | Interacts with M protein to regulate PEDV replication, viral protein synthesis, and assembly |
| EGFR | Regulates endocytic transport; regulates sorting after internalization and endocytosis | Inhibits I-IFN response through STAT3-mediated signaling |
Transmission by direct and indirect contact is the main route of PEDV transmission between pigs. PEDV is transmitted between pigs at different ages and usually first infects finishing pigs, then the virus spreads to pregnant sows in the farrowing house, and subclinically infected sows then transmit PEDV to suckling piglets, eventually causing an epidemic of high mortality in piglets. Here, we summarize several routes of PEDV transmission between pigs. PEDV spreads in several different ways during infection, and one of the most common is the fecal–oral route, that is, direct or indirect transmission through porcine feces, vomit, and other contaminants produced by the livestock process. PEDV can be infected through the route of transmission from porcine feces to the nasal cavity, known as the fecal–nasal route. In addition, PEDV can also be transmitted vertically to piglets through sow milk.
Figure 2. Several transmission routes of PEDV infection. (Zhang, Yuanzhu,et al, 2022)
PEDV was first reported in the 1970s in the UK and Belgium, and as early as the 1980s. Until 2010, PEDV strains from the classical subgroup (GIa) caused widespread outbreaks in East Asia, but there were only sporadic and localized PED cases in China. Since October 2010, the PEDV strain of GIIa subgroup PEDV has caused a large-scale outbreak of PED. Even pigs vaccinated with inactivated tissue vaccine, inactivated CV777 vaccine, and inactivated or attenuated bivalent vaccine (porcine epidemic diarrhea virus+porcine coronavirus) have not been spared, and the incidence rate and mortality rate are almost 100%. Then the epidemic immediately spread to all parts of the country, causing devastating damage to China's pig industry. Since 2013, a highly lethal PEDV has emerged in North America, classified as the GIIb subgroup, and soon after, it quickly swept across multiple countries around the world. After the outbreak of the GIIb strain, a new variant emerged in the United States, characterized by deletion and insertion of nucleic acid sequences in the S gene, classified as S-INDEL.
The high morbidity and high mortality that PEDV brings to piglets results in a rapid transmission of PEDV in pig populations, which has brought huge economic losses to the global swine industry. Considering the hazards caused by PEDV, preventive immunization is administered by vaccinating pregnant sows. However, due to the high heterogeneity of PEDV, there are currently no effective and safe vaccines to deal with the threat posed by PEDV. Exploring the genetic variation of PEDV and its virulence changes will help us to have a deeper understanding of PEDV and take more efficient diagnosis and treatment measures, accordingly.
Reference
| Target | Cat. No. | Product Name | Host | Isotype | Application | |
| PEDV | DPAB-CS24090 | Porcine Anti-PEDV Control Serum | Porcine | IgG | IF | Inquiry |
| CABT-L0933X | Rabbit Anti-PEDV S2 polyclonal antibody | Rabbit | IgG | ELISA, IHC, WB | Inquiry | |
| CABT-BL8885 | Mouse Anti-Porcine Epidemic Diarrhea Virus Monoclonal Antibody, clone 3G8 | Mouse | IgG1 | ELISA(Det) | Inquiry | |
| CABT-BL8886 | Mouse Anti-Porcine Epidemic Diarrhea Virus Monoclonal Antibody, clone 4E7 | Mouse | IgG1 | ELISA(Cap) | Inquiry | |
| CABT-BL8956 | Anti-PEDV monoclonal antibody | Mouse | IgG2a | IFA | Inquiry | |
| CABT-BL8958 | Anti-PPV monoclonal antibody | Mouse | IgG1 | Neut, IFA, HI, RIA, IHC | Inquiry | |
| CABT-B8970 | Anti-PEDV monoclonal antibody, clone 3G8D0 | Mouse | IgG1 | ELISA, WB | Inquiry | |
| PEFV NP | DPAB-CS24584 | Rabbit Anti-PEDV NP Polyclonal antibody | Rabbit | IgG | ELISA | Inquiry |
| PEDV S1 | DMAB-CS23088 | Mouse Anti-PEDV S1 Monoclonal antibody, clone QX1101 | Mouse | IgG | ELISA | Inquiry |
| PEDV S2 | DMAB-CS23089 | Mouse Anti-PEDV S2 Monoclonal antibody, clone QX1102 | Mouse | IgG | ELISA | Inquiry |
| PEDV NP | DMAB-CS23090 | Mouse Anti-PEDV NP Monoclonal antibody, clone QX1103 | Mouse | IgG | ELISA | Inquiry |
| Target | Cat. No. | Product Name | Host | |
| PEDV | DAG-WT5852 | Porcine epidemic diarrhea virus (PEDV) Stock (Qualitative) | N/A | Inquiry |
| DAG-WT237 | Recombinant PEDV S1 Protein [His] | Mammalian cells | Inquiry | |
| DAG-WT1129 | Inactivated PEDV Antigen | N/A | Inquiry | |
| DAG-WT2271 | Recombinant PEDV Nucleocapsid Protein [His] | E. coli | Inquiry |
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