ArticleJournal of virology2017
The Nucleocapsid Protein and Nonstructural Protein 10 of Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus Enhance CD83 Production via NF-κB and Sp1 Signaling Pathways.
Article in Journal of virology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 42 citations in OpenAlex.
- Article
- PRRSV suppresses FTO-dependentmBio · 2026Article
- The mRNA and protein of IL-8 oppositely regulate PRRSV replication via nucleoprotein and 14-3-3γ.Journal of virology · 2025Article
- Immune Protection Gap Between Porcine Reproductive and Respiratory Syndrome Subunit Vaccine (N Protein) and Live Vaccine.Vaccines · 2025Article
- Calcium-mediated mitochondrial fission and mitophagy drive glycolysis to facilitate arterivirus proliferation.PLoS pathogens · 2025Article
- Research Progress on the NSP10 Protein of Porcine Reproductive and Respiratory Syndrome Virus.Microorganisms · 2024Review
- Research progress on the N protein of porcine reproductive and respiratory syndrome virus.Frontiers in microbiology · 2024Review
- Article
- Article
- Porcine reproductive and respiratory syndrome virus infection triggers autophagy via ER stress-induced calcium signaling to facilitate virus replication.PLoS pathogens · 2023Article
- Signaling Lymphocytic Activation Molecule Family Member 1 Inhibits Porcine Reproductive and Respiratory Syndrome Virus Replication.Animals : an open access journal from MDPI · 2022Article
- A New Long Noncoding RNA, MAHAT, Inhibits Replication of Porcine Reproductive and Respiratory Syndrome Virus by Recruiting DDX6 To Bind toJournal of virology · 2022Article
- A novel amino acid site of N protein could affect the PRRSV-2 replication by regulating the viral RNA transcription.BMC veterinary research · 2022Article
- Role of transcription factors in porcine reproductive and respiratory syndrome virus infection: A review.Frontiers in microbiology · 2022Review
- Chitosan-Coated Selenium Nanoparticles Attenuate PRRSV Replication and ROS/JNK-Mediated Apoptosis in vitro.International journal of nanomedicine · 2022Article
- Potential Molecular Mechanisms and Remdesivir Treatment for Acute Respiratory Syndrome Corona Virus 2 Infection/COVID 19 Through RNA Sequencing and Bioinformatics Analysis.Bioinformatics and biology insights · 2021Article
- Article
- Porcine Reproductive and Respiratory Syndrome Virus Enhances Self-Replication via AP-1-Dependent Induction of SOCS1.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- S100A9 regulates porcine reproductive and respiratory syndrome virus replication by interacting with the viral nucleocapsid protein.Veterinary microbiology · 2019Article
- Nuclear localization signal in TRIM22 is essential for inhibition of type 2 porcine reproductive and respiratory syndrome virus replication in MARC-145 cells.Virus genes · 2019Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Porcine reproductive and respiratory syndrome, caused by porcine reproductive and respiratory syndrome virus (PRRSV), is a panzootic disease that is one of the most economically costly diseases to the swine industry. A key aspect of PRRSV virulence is that the virus suppresses the innate immune response and induces persistent infection, although the underlying mechanisms are not well understood. The dendritic cell (DC) marker CD83 belongs to the immunoglobulin superfamily and is associated with DC activation and immunosuppression of T cell proliferation when expressed as soluble CD83 (sCD83). In this study, we show that PRRSV infection strongly stimulates CD83 expression in porcine monocyte-derived DCs (MoDCs) and that the nucleocapsid (N) protein and nonstructural protein 10 (nsp10) of PRRSV enhance CD83 promoter activity via the NF-κB and Sp1 signaling pathways. R43A and K44A amino acid substitution mutants of the N protein suppress the N protein-mediated increase of CD83 promoter activity. Similarly, P192-5A and G214-3A mutants of nsp10 (with 5 and 3 alanine substitutions beginning at residues P192 and G214, respectively) abolish the nsp10-mediated induction of the CD83 promoter. Using reverse genetics, four mutant viruses (rR43A, rK44A, rP192-5A, and rG214-3A) and four revertants [rR43A(R), rK44A(R), rP192-5A(R), and rG214-3A(R)] were generated. Decreased induction of CD83 in MoDCs was observed after infection by mutants rR43A, rK44A, rP192-5A, and rG214-3A, in contrast to the results obtained using rR43A(R), rK44A(R), rP192-5A(R), and rG214-3A(R). These findings suggest that PRRSV N and nsp10 play important roles in modulating CD83 signaling and shed light on the mechanism by which PRRSV modulates host immunity.
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