ArticleVirology journal2018
RIG-I is responsible for activation of type I interferon pathway in Seneca Valley virus-infected porcine cells to suppress viral replication.
Article in Virology journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 22 citations in OpenAlex.
- Determinants of Senecavirus A Pathogenesis: From Viral Genome to ANTXR1, Immunity, and Programmed Cell Death.Viruses · 2026Review
- Dysregulation of RIG-I activation by picornavirus 3A protein.Journal of virology · 2026Article
- The Seneca Valley virus 3C protease cleaves DCP1A to attenuate its antiviral effects.Veterinary research · 2025Article
- TRIM5 inhibits the replication of Senecavirus A by promoting the RIG-I-mediated type I interferon antiviral response.Veterinary research · 2024Article
- Dampening of ISGylation of RIG-I by ADAP regulates type I interferon response of macrophages to RNA virus infection.PLoS pathogens · 2024Article
- Review
- Development of Specific Monoclonal Antibodies against Porcine RIG-I-like Receptors Revealed the Species Specificity.International journal of molecular sciences · 2023Article
- Successful Treatment of SARS-CoV-2 Vaccination-related Activation of Rheumatoid Arthritis with Positive Findings for Epstein-Barr Virus.Internal medicine (Tokyo, Japan) · 2022Article
- Article
- Mfn2 is responsible for inhibition of the RIG-I/IRF7 pathway and activation of NLRP3 inflammasome in Seneca Valley virus-infected PK-15 cells to promote viral replication.Frontiers in immunology · 2022Article
- Transcriptome Analyses of Senecavirus A-Infected PK-15 Cells: RIG-I and IRF7 Are the Important Factors in Inducing Type III Interferons.Frontiers in microbiology · 2022Article
- Interferon responses to norovirus infections: current and future perspectives.The Journal of general virology · 2021Review
- Review
- Construction and Generation of a Recombinant Senecavirus a Stably Expressing the NanoLuc Luciferase for Quantitative Antiviral Assay.Frontiers in microbiology · 2021Article
- UMP-CMP kinase 2 gene expression in macrophages is dependent on the IRF3-IFNAR signaling axis.PloS one · 2021Article
- Porcine RIG-I and MDA5 Signaling CARD Domains Exert Similar Antiviral Function Against Different Viruses.Frontiers in microbiology · 2021Article
- Analysis of Porcine RIG-I Like Receptors Revealed the Positive Regulation of RIG-I and MDA5 by LGP2.Frontiers in immunology · 2021Article
- E2 ubiquitin-conjugating enzyme UBE2L6 promotes Senecavirus A proliferation by stabilizing the viral RNA polymerase.PLoS pathogens · 2020Article
- Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundRetinoic acid-inducible gene I (RIG-I) is a key cytosolic receptor of the innate immune system. Seneca valley virus (SVV) is a newly emerging RNA virus that infects pigs causing significant economic losses in pig industry. RIG-I plays different roles during different viruses infections. The role of RIG-I in SVV-infected cells remains unknown. Understanding of the role of RIG-I during SVV infection will help to clarify the infection process of SVV in the infected cells.
methodsIn this study, we generated a RIG-I knockout (KO) porcine kidney PK-15 cell line using the Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)/CRISPR-associated protein-9 nuclease (Cas9) genome editing tool. The RIG-I gene sequence of RIG-I KO cells were determined by Sanger sequencing method, and the expression of RIG-I protein in the RIG-I KO cells were detected by Western bloting. The activation status of type I interferon pathway in Sendai virus (SeV)- or SVV-infected RIG-I KO cells was investigated by measuring the mRNA expression levels of interferon (IFN)-β and IFN-stimulated genes (ISGs). The replicative state of SVV in the RIG-I KO cells was evaluated by qPCR, Western bloting, TCID
resultsGene editing of RIG-I in PK-15 cells successfully resulted in the destruction of RIG-I expression. RIG-I KO PK-15 cells had a lower expression of IFN-β and ISGs compared with wildtype (WT) PK-15 cells when stimulated by the model RNA virus SeV. The amounts of viral RNA and viral protein as well as viral yields in SVV-infected RIG-I WT and KO cells were determined and compared, which showed that knockout of RIG-I significantly increased SVV replication and propagation. Meanwhile, the expression of IFN-β and ISGs were considerably decreased in RIG-I KO cells compared with that in RIG-I WT cells during SVV infection.
conclusionAltogether, this study indicated that RIG-I showed an antiviral role against SVV and was essential for activation of type I IFN signaling during SVV infection. In addition, this study suggested that the CRISPR/Cas9 system can be used as an effective tool to modify cell lines to increase viral yields during SVV vaccine development.
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