ArticleVeterinary research2017
Identification of two mutation sites in spike and envelope proteins mediating optimal cellular infection of porcine epidemic diarrhea virus from different pathways.
Article in Veterinary research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 35 citations in OpenAlex.
- How Does Porcine Epidemic Diarrhea Virus Escape Host Innate Immunity?Pathogens (Basel, Switzerland) · 2025Review
- The effect of asparagine-13 in porcine epidemic diarrhea virus envelope protein on pathogenicity.Veterinary research · 2025Article
- Isolation and pathogenicity of a variant porcine epidemic diarrhea virus field strain with high adaptability to Vero cell.Frontiers in veterinary science · 2025Article
- Molecular detection and evolutionary analysis of porcine epidemic diarrhea virus in Henan and Shaanxi provinces in China.Archives of virology · 2024Article
- Genetic characteristics associated with the virulence of porcine epidemic diarrhea virus (PEDV) with a naturally occurring truncated ORF3 gene.Veterinary research · 2024Article
- Developing Next-Generation Live Attenuated Vaccines for Porcine Epidemic Diarrhea Using Reverse Genetic Techniques.Vaccines · 2024Review
- Deletion of a 7-amino-acid region in the porcine epidemic diarrhea virus envelope protein induces higher type I and III interferon responses and results in attenuationJournal of virology · 2023Article
- Natural Evolution of Porcine Epidemic Diarrhea Viruses Isolated from Maternally Immunized Piglets.Animals : an open access journal from MDPI · 2023Article
- Coronavirus and the Cytoskeleton of Virus-Infected Cells.Sub-cellular biochemistry · 2023Article
- Construction and immunogenicity of a trypsin-independent porcine epidemic diarrhea virus variant.Frontiers in immunology · 2023Article
- Screening Host Antiviral Proteins under the Enhanced Immune Responses Induced by a Variant Strain of Porcine Epidemic Diarrhea Virus.Microbiology spectrum · 2022Article
- The Effects of Swine Coronaviruses on ER Stress, Autophagy, Apoptosis, and Alterations in Cell Morphology.Pathogens (Basel, Switzerland) · 2022Review
- Interplay between swine enteric coronaviruses and host innate immune.Frontiers in veterinary science · 2022Review
- Article
- Does Trypsin Oral Spray (ViruprotectInternational journal of environmental research and public health · 2021Article
- The trypsin-enhanced infection of porcine epidemic diarrhea virus is determined by the S2 subunit of the spike glycoprotein.Journal of virology · 2021Article
- Porcine Epidemic Diarrhea Virus Envelope Protein Blocks SLA-DR Expression in Barrow-Derived Dendritic Cells by Inhibiting Promoters Activation.Frontiers in immunology · 2021Article
- Systemic and Oral Immunogenicity of Porcine Epidemic Diarrhea Virus Antigen Fused to Poly-Fc of Immunoglobulin G and Expressed in ΔXT/FTFrontiers in pharmacology · 2021Article
- Porcine epidemic diarrhea virus: Molecular mechanisms of attenuation and vaccines.Microbial pathogenesis · 2020Review
- Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Entry of the α-coronavirus porcine epidemic diarrhea virus (PEDV) requires specific proteases to activate spike (S) protein for the membrane fusion of the virion to the host cell following receptor binding. Herein, PEDV isolate 85-7 could proliferate and induce cell-cell fusion in a trypsin independent manner on Vero cells, and eight homologous mutation strains were screened by continuous proliferation in the absence of trypsin on Vero cells. According to the whole genome sequence comparative analysis, we identified four major variations located in nonstructural protein 2, S, open reading frame 3, and envelope (E) genes, respectively. Comparative analyses of their genomic variations and proliferation characteristics identified a single mutation within the S2' cleavage site between C30 and C40 mutants: the substitution of conserved arginine (R) by a glycine (G) (R895G). This change resulted in weaker cell-cell fusion, smaller plaque morphology, higher virus titer and serious microfilament condensation. Further analysis confirmed that this mutation was responsible for optimal cell-adaptation, but not the determinant for trypsin-dependent entry of PEDV. Otherwise, a novel variation (16-20 aa deletion and an L25P mutation) in the transmembrane domain of the E protein affected multiple infection processes, including up-regulation of the production of the ER stress indicator GRP78, improving the expression of pro-inflammatory cytokines IL-6 and IL-8, and promoting apoptosis. The results of this study provide a better understanding of the potential mechanisms of viral functional proteins in PEDV replication, infection, and fitness.
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