ArticleVirology journal2017
Porcine Viperin protein inhibits the replication of classical swine fever virus (CSFV) in vitro.
Article in Virology journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Gene Editing for Enhanced Swine Production: Current Advances and Prospects.Animals : an open access journal from MDPI · 2025Review
- Advances in CRISPR/Cas-Based Strategies on Zoonosis.Transboundary and emerging diseases · 2023Review
- Pestiviruses infection: Interferon-virus mutual regulation.Frontiers in cellular and infection microbiology · 2023Review
- Review
- Anti-Classical Swine Fever Virus Strategies.Microorganisms · 2021Review
- Viperin: An ancient radical SAM enzyme finds its place in modern cellular metabolism and innate immunity.The Journal of biological chemistry · 2020Review
- Antiviral activity of ISG15 against classical swine fever virus replication in porcine alveolar macrophages via inhibition of autophagy by ISGylating BECN1.Veterinary research · 2020Article
- Structural Basis of the Substrate Selectivity of Viperin.Biochemistry · 2020Article
- Head Start Immunity: Characterizing the Early Protection of C Strain Vaccine Against Subsequent Classical Swine Fever Virus Infection.Frontiers in immunology · 2019Article
- IFN-Lambda 3 Mediates Antiviral Protection Against Porcine Epidemic Diarrhea Virus by Inducing a Distinct Antiviral Transcript Profile in Porcine Intestinal Epithelia.Frontiers in immunology · 2019Article
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundClassical swine fever virus (CSFV) is the causative pathogen of Classical swine fever (CSF), a highly contagious disease of swine. Viperin is one of the hundreds of interferon-stimulated genes (ISGs), and possesses a wide range of antiviral activities. The aim of this study was to explore whether porcine Viperin has the anti-CSFV activity.
methodThe influences of CSFV infection on Viperin expression and Newcastle disease virus (NDV)/Pseudorabies virus (PRV)-induced Viperin expression were examined in 3D4/21 cells and porcine peripheral blood mononuclear cells (PBMCs). Porcine Viperin gene was amplified to generate cell line PK-Vi over-expressing Viperin. CSFV was inoculated in the cell lines and viral load was detected by qRT-PCR, virus titration and Western blot. The influence of Viperin expression on CSFV binding, entry and release in the cells was also examined. The co-localization of Viperin with CSFV and its proteins (E2, NS5B) was determined by confocal laser scanning microscopy test. Co-IP assay was performed to check the interaction of Viperin with CSFV proteins.
resultsCSFV infection could not induce Viperin expression in vitro while significantly inhibiting NDV/PRV-induced Viperin expression at 12, 24 and 48 h post infection (hpi; P < 0.05). The proliferation of CSFV in PK-Vi was significantly inhibited at 24, 48 and 72 hpi (P < 0.05), comparing with control cells (PK-C1 expressing EGFP). Virus in both cell culture supernatants and cell pellets were reduced equally. CSFV binding and entry in the cells were not interfered by Viperin expression. These results indicated its anti-CSFV function occurred during the genome and/or protein synthesis step. Confocal laser scanning microscopy test showed the Viperin-EGFP protein co-localized with CSFV E2 protein in CSFV infected PK-Vi cells. Further experiments indicated that Viperin protein co-localized with E2 and NS5B proteins of CSFV in the transfected 293 T cells. Furthermore, Co-IP assay confirmed the interaction of Viperin with E2 protein, but not NS5B.
conclusionPorcine Viperin effectively inhibited CSFV replication in vitro, potentially via the interaction of Viperin with CSFV E2 protein in cytoplasm. The results provided foundation for further studies of the interaction of Viperin with CSFV and other viruses.
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