Porcine epidemic diarrhea virus: Molecular mechanisms of attenuation and vaccines

Abstract

Porcine epidemic diarrhea virus (PEDV) causes an emerging and re-emerging coronavirus disease characterized by vomiting, acute diarrhea, dehydration, and up to 100% mortality in neonatal suckling piglets, leading to huge economic losses in the global swine industry. Vaccination remains the most promising and effective way to prevent and control PEDV. However, effective vaccines for PEDV are still under development. Understanding the genomic structure and function of PEDV and the influence of the viral components on innate immunity is essential for developing effective vaccines. In the current review, we systematically describe the recent developments in vaccine against PEDV and the roles of structural proteins, non-structural proteins and accessory proteins of PEDV in affecting viral virulence and regulating innate immunity, which will provide insight into the rational design of effective and safe vaccines for PEDV or other coronaviruses.

Keywords: Genetics; Porcine epidemic diarrhea virus; Vaccine; Virulence.

Fig. 1

(a) Schematic structure of the virion of PEDV. (b) Schematic diagram of the genome of PEDV. Structural proteins, including spike (S), envelope (E), membrane (M) and nucleocapsid (N) proteins, as well as accessory proteins ORF3 and non-structural proteins derived from ppl1ab, including nsp1-16, papain-like proteinase (PLpro, nsp3), 3C-like proteinase (3CLpro, nsp5), RNA-dependent RNA polymerase (RdRp, nsp12), 5′-to-3′ Helicase (HEL, nsp13), exoribonuclease (ExoN, nsp14), endoribonuclease (EndoU, nsp15), 2′-O-methyltransferases (2′-O-MTase, nsp16). Spike protein, including signal peptide (SP, 1–18 aa), sialic acid-binding region (SIA, 19–233 aa), core neutralizing epitope (COE, 499–638 aa), fusion peptide (FP, 891–908 aa), heptad repeat domain (HR1, 978–1117 aa and HR2, 1274–1313 aa), transmembrane domain (TM, 1328–1350 aa), and cytoplasmic domain (CP, 1351–1386 aa).