Porcine Epidemic Diarrhea Virus Background

PEDV disease was first reported in England and Belgium in the late 1970s and has since been observed worldwide, causing significant economic losses. In the US the disease is caused by two different genogroups (G) of PEDV, S INDEL [PEDV variant containing multiple deletions and insertions in the S1 subunit of the spike (S) protein, G1b] and non-S INDEL (G2b) strains (Jung et al., 2020). PEDV is enveloped, pleomorphic and 95–190 nm in diameter, including the projections, which are approximately 18 nm in length. PEDV has a single-stranded positive-sense RNA genome of approximately 28 kb in size (excluding the poly A-tail) that encodes four structural proteins, namely, S, envelope (E), membrane (M) and nucleocapsid (N) proteins, sixteen nonstructural proteins (nsp1-nsp16) and an accessory protein ORF3. The S protein is critical for interactions with the specific host cell receptor to mediate viral binding and entry and for inducing neutralizing antibodies. The S protein is divided into S1 and S2 subunits. The N-terminal S1 subunit contains the receptor binding domain and the C-terminal S2 subunit is responsible for membrane fusion. The accessory protein ORF3 is an ion channel protein and is dispensable for virus replication in vitro (Jung et al., 2020)..

The fecal–oral route is the main means of direct transmission of PEDV via the feces and/or vomitus of infected pigs but indirect contact transmission of PEDV is also frequent. The fecal–nasal route is another route of pig-to-pig, or farm-to-farm (up to 10 miles away) airborne transmission of PEDV via aerosolized PEDV particles that are infectious in nursing pigs. Cross-contamination during feed manufacturing can also occur. The incubation period is estimated to be between 1 and 4 days and the infectious period can last between 6 and 35 days after the first onset of clinical signs. Duration of diarrhea in infected nursing pigs varies from 2 to 8 days (Jung et al., 2020). PEDV infects the cells lining the small intestine of a pig. During acute PEDV infection PEDV initially infects the mid-jejunum and ileum and to a lesser extent, the proximal and distal jejunum and duodenum. Porcine small intestinal villous enterocytes express aminopeptidase N (APN), a 150-kDa glycosylated transmembrane protein, which acts as a cellular receptor for PEDV. However, it may not be the major cell surface receptor for PEDV. Cell membrane cholesterol or two cell surface molecules, such as sialic acids and occludin expressed on the apical surface of secretary (goblet) or absorptive enterocytes, respectively, have also been shown to be involved partially in binding and entry of PEDV into enterocytes (Jung et al., 2020).

Porcine enteric coronaviruses which are clinically similar to PEDV (e.g. transmissible gastroenteritis virus (TGEV), porcine respiratory coronavirus (PRCV), porcine deltacoronavirus (PDCoV) and swine acute diarrhea syndrome coronavirus (SADS-CoV)) display clinical signs which are indistinguishable from each other and differential diagnosis is therefore critical to control these diseases in pigs. There have been increased reports since 2011 regarding high morbidity and mortality, particularly in young pigs. In outbreaks described in 2013 and 2014, mortalities in suckling piglets ranged from 50 to 100% at the farm level (OIE, 2014).

References

• Jung K, Saif LJ, Wang Q. Porcine epidemic diarrhea virus (PEDV): An update on etiology, transmission, pathogenesis, and prevention and control. Virus Res. 2020 Sep;286:198045.
• OIE Technical Factsheet. Infection with Porcine Epidemic Diarrhoea Virus. 2014.