ArticleJournal of virology2018
Nsp1α of Porcine Reproductive and Respiratory Syndrome Virus Strain BB0907 Impairs the Function of Monocyte-Derived Dendritic Cells via the Release of Soluble CD83.
Article in Journal of virology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- PRRSV suppresses FTO-dependentmBio · 2026Article
- Highly pathogenic porcine reproductive and respiratory syndrome virus nonstructural protein 1 interacts with TRAF6 to activate the TAK1/p38/JNK/AP-1 signaling and induce IL-1β.Journal of virology · 2026Article
- Discovery of a [4Fe-4S] cluster in the PRRSV Nsp1α leader protease reveals host-virus interplay in its downstream functions.Science advances · 2026Article
- NPRL2 restricts porcine reproductive and respiratory syndrome virus replication by targeting viral Nsp1α for autophagic degradation.Veterinary research · 2026Article
- Discovery of a [4Fe-4S] cluster in the PRRSV Nsp1α leader protease reveals host-virus interplay in its downstream functions.bioRxiv : the preprint server for biology · 2026Article
- Self-assembled cyanidin-3-O-glucoside nanoparticles alleviate inflammation and ferroptosis induced by PRRSV infection.Journal of virology · 2025Article
- Strategies and scheming: the war between PRRSV and host cells.Virology journal · 2025Review
- The dimeric conformation of PRRSV nsp1α is important for its ability to regulate viral RNA synthesis.Veterinary research · 2025Article
- Vidofludimus inhibits porcine reproductive and respiratory syndrome virus infection by targeting dihydroorotate dehydrogenase.Veterinary research · 2023Article
- Article
- A New Long Noncoding RNA, MAHAT, Inhibits Replication of Porcine Reproductive and Respiratory Syndrome Virus by Recruiting DDX6 To Bind toJournal of virology · 2022Article
- Article
- Broadly Antiviral Activities of TAP1 through Activating the TBK1-IRF3-Mediated Type I Interferon Production.International journal of molecular sciences · 2021Article
- S100A9 regulates porcine reproductive and respiratory syndrome virus replication by interacting with the viral nucleocapsid protein.Veterinary microbiology · 2019Article
- Xanthohumol inhibits PRRSV proliferation and alleviates oxidative stress induced by PRRSV via the Nrf2-HMOX1 axis.Veterinary research · 2019Article
- ZAP, a CCCH-Type Zinc Finger Protein, Inhibits Porcine Reproductive and Respiratory Syndrome Virus Replication and Interacts with Viral Nsp9.Journal of virology · 2019Article
- Cellular Innate Immunity against PRRSV and Swine Influenza Viruses.Veterinary sciences · 2019Review
- Key Gaps in the Knowledge of the Porcine Respiratory Reproductive Syndrome Virus (PRRSV).Frontiers in veterinary science · 2019Review
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 virus (PRRSV), a virulent pathogen of swine, suppresses the innate immune response and induces persistent infection. One mechanism used by viruses to evade the immune system is to cripple the antigen-processing machinery in monocyte-derived dendritic cells (MoDCs). In this study, we show that MoDCs infected by PRRSV express lower levels of the major histocompatibility complex (MHC)-peptide complex proteins TAP1 and ERp57 and are impaired in their ability to stimulate T cell proliferation and increase their production of CD83. Neutralization of sCD83 removes the inhibitory effects of PRRSV on MoDCs. When MoDCs are incubated with exogenously added sCD83 protein, TAP1 and ERp57 expression decreases and T lymphocyte activation is impaired. PRRSV nonstructural protein 1α (Nsp1α) enhances CD83 promoter activity. Mutations in the ZF domain of Nsp1α abolish its ability to activate the CD83 promoter. We generated recombinant PRRSVs with mutations in Nsp1α and the corresponding repaired PRRSVs. Viruses with Nsp1α mutations did not decrease levels of TAP1 and ERp57, impair the ability of MoDCs to stimulate T cell proliferation, or increase levels of sCD83. We show that the ZF domain of Nsp1α stimulates the secretion of CD83, which in turn inhibits MoDC function. Our study provides new insights into the mechanisms of immune suppression by PRRSV.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.