Abstract
Porcine epidemic diarrhea virus (PEDV) causes continuous, significant damage to the swine industry worldwide. By RT-PCR-based methods, this study demonstrated the ongoing presence of PEDV in pigs of all ages in Korea at the average detection rate of 9.92%. By the application of Bayesian phylogenetic analysis, it was found that the nucleocapsid (N) gene of PEDV could evolve at similar rates to the spike (S) gene at the order of 10−4 substitutions/site/year. Based on branching patterns of PEDV strains, three main N gene-base genogroups (N1, N2, and N3) and two sub-genogroups (N3a, N3b) were proposed in this study. By analyzing the antigenic index, possible antigenic differences also emerged in both the spike and nucleocapsid proteins between the three genogroups. The antigenic indexes of genogroup N3 strains were significantly lower compared with those of genogroups N1 and N2 strains in the B-cell epitope of the nucleocapsid protein. Similarly, significantly lower antigenic indexes in some parts of the B-cell epitope sequences of the spike protein (COE, S1D, and 2C10) were also identified. PEDV mutants derived from genetic mutations of the S and N genes may cause severe damage to swine farms by evading established host immunities.
Highlights
Porcine epidemic diarrhea virus (PEDV) is an enveloped, single-stranded RNA virus belonging to the family Coronaviridae, subfamily Coronavirinae, genus Alphacoronavirus, and subgenus Pedacovirus
PEDV is one of the major pathogens causing acute enteritis disease, which is characterized by vomiting and watery diarrhea and commonly leads to high rates of mortality and morbidity in suckling piglets [1]
Since the 1980s, PEDV has been widespread throughout Asia, where it has been regarded as an endemic disease for many years [3,4]
Summary
PEDV is one of the major pathogens causing acute enteritis disease, which is characterized by vomiting and watery diarrhea and commonly leads to high rates of mortality and morbidity in suckling piglets [1]. The disease was first reported in the UK in 1971, and the prototype virus—designated as PEDV CV777—was subsequently identified in Belgium [2]. In the late 2010s, new and highly pathogenic strains were reported in China. These new strains were pathologically more critical than the classic strains, resulting in morbidities of 80–100% and mortality rates of 50–100% in infected suckling piglets [5]. In May 2013, these new highly pathogenic strains
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