US variant porcine epidemic diarrhea virus: histological lesions and genetic characterization

Abstract

Porcine epidemic diarrhea virus (PEDV) was first recognized in pigs in the United States (US) in May 2013. Since then, the virus has spread to over 30 states and caused significant economic losses in the US swine industry due to the high mortality in newborn piglets less than 2 weeks of age. A mild-variant strain OH851 of PEDV in the US was first reported in January 2014. Here, we report histological changes in the small intestines of five piglets infected with the variant strain OH851 of PEDV. The lesions observed were milder, compared to the US classical strain of PEDV. Our study, for the first time, reports the histological lesions caused by the variant PEDV OH851 strain from a field case. In addition, genomic characterization demonstrated that US variant PEDV is more closely related to European-like strains in the first 1170 nt of the 5' spike gene but to US classical PEDV strains in the remaining genome, suggesting that the variant PEDV strain may derive from a recombinant event between the US classical and European-like PEDV strains.

Differential gene modulation of pattern-recognition receptor TLR and RIG-I-like and downstream mediators on intestinal mucosa of pigs infected with PEDV non S-INDEL and PEDV S-INDEL strains

“…Porcine epidemic diarrhea virus (PEDV) causes enteric diseases, resulting in significant economic losses. PEDV pathogenesis is strainspecific, and pathogenesis studies in neonatal pigs have demonstrated that the PEDV non-S-INDEL strain is more pathogenic than the PEDV S-INDEL strain Wang et al, 2016;Yamamoto et al, 2015). PEDV S-INDEL was shown to be clinically relevant in neonates, but clinical disease could not be reproduced in pigs older than three weeks (Annamalai et al, 2015;Chen et al, 2016).…”

“…On the basis of differences in the S gene and virulence, emerging PEDV strains can be divided into non-S-INDEL (S gene insertions and deletions) and S-INDEL strains (Vlasova et al, 2014). PEDV pathogenesis is strain-specific, and pathogenesis studies in neonatal pigs have demonstrated that the PEDV non-S-INDEL strain is more pathogenic than the PEDV S-INDEL strain Wang et al, 2016;Yamamoto et al, 2015). PEDV pathogenesis is also inversely correlated with the age of the animals.…”

Isolation and Identification of Porcine Epidemic Diarrhea Virus and Its Effect on Host Natural Immune Response

“…The pathogenesis of PEDV is strain specific. Studies on its pathogenesis in piglets suggest that the PEDV non-S-INDEL strain has stronger pathogenicity compared to the PEDV S-INDEL strain (Chen et al, 2014; Yamamoto et al, 2015; Wang et al, 2016). PEDV JS-A belongs to the non-S-INDEL strain.…”

Short communication: antiviral activity of porcine IFN-λ3 against porcine epidemic diarrhea virus in vitro

“…Previous studies have demonstrated that IFNks can induce protection against several viruses in cell culture, such as West Nile virus [16], influenza A virus [10], porcine reproductive and respiratory syndrome virus [15], and foot-and-mouth disease virus [5]. Porcine epidemic diarrhea virus (PEDV) is a member of the family Coronaviridae, and is an important etiological agent of lethal watery diarrhea in piglets, resulting in large economic losses in many Asian and European countries [23,24]. Previous research has demonstrated that PEDV infection suppresses the production of IFN-b, and viral papain-like protease 2 has been identified as a type I interferon antagonist [4,6,24,25].…”

“…Porcine epidemic diarrhea virus (PEDV) is a member of the family Coronaviridae, and is an important etiological agent of lethal watery diarrhea in piglets, resulting in large economic losses in many Asian and European countries [23,24]. Previous research has demonstrated that PEDV infection suppresses the production of IFN-b, and viral papain-like protease 2 has been identified as a type I interferon antagonist [4,6,24,25]. In this study, poIFN-k3 was cloned and expressed in Escherichia coli using the pET-32a vector.…”