ArticleJournal of virology2019
Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus Induces Interleukin-17 Production via Activation of the IRAK1-PI3K-p38MAPK-C/EBPβ/CREB Pathways.
Article in Journal of virology, 2019. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- PRRSV infection induces mitochondrial damage and releases mitochondrial dsRNA to activate the NLRP3-dependent inflammatory response.Veterinary research · 2026Article
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- Strategies and scheming: the war between PRRSV and host cells.Virology journal · 2025Review
- Early boosting of p38 MAPK signaling pathway by lycorine hydrochloride potently inhibits PRRSV proliferation in primary and established cells.Frontiers in microbiology · 2025Article
- Type I and II interferons, transcription factors and major histocompatibility complexes were enhanced by knocking down the PRRSV-induced transforming growth factor beta in monocytes co-cultured with peripheral blood lymphocytes.Frontiers in immunology · 2024Article
- Research Progress on NSP11 of Porcine Reproductive and Respiratory Syndrome Virus.Veterinary sciences · 2023Review
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- Genetic background influences pig responses to porcine reproductive and respiratory syndrome virus.Frontiers in veterinary science · 2023Review
- Role of transcription factors in porcine reproductive and respiratory syndrome virus infection: A review.Frontiers in microbiology · 2022Review
- Th17 cell differentiation induced by cytopathogenic biotype BVDV-2 in bovine PBLCs.BMC genomics · 2021Article
- Andrographolide and Its Derivative Potassium Dehydrographolide Succinate Suppress PRRSV Replication in Primary and Established Cells via Differential Mechanisms of Action.Virologica Sinica · 2021Article
- The C/EBPβ-Dependent Induction of TFDP2 Facilitates Porcine Reproductive and Respiratory Syndrome Virus Proliferation.Virologica Sinica · 2021Article
- Porcine Reproductive and Respiratory Syndrome Virus nsp11 Antagonizes Broad Antiviral Effects of MCPIP1 by Inducing Interleukin-17 Expression.Journal of virology · 2021Article
- The Function of the PRRSV-Host Interactions and Their Effects on Viral Replication and Propagation in Antiviral Strategies.Vaccines · 2021Review
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- PPRV-induced novel miR-3 contributes to inhibit type I IFN production by targeting IRAK1.Journal of virology · 2021Article
- Molecular and Cellular Mechanisms for PRRSV Pathogenesis and Host Response to Infection.Virus research · 2020Review
- Intranasal Delivery of Inactivated Influenza Virus and Poly(I:C) Adsorbed Corn-Based Nanoparticle Vaccine Elicited Robust Antigen-Specific Cell-Mediated Immune Responses in Maternal Antibody Positive Nursery Pigs.Frontiers in immunology · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Porcine reproductive and respiratory syndrome virus (PRRSV) is widely prevalent in pigs, resulting in significant economic losses worldwide. A compelling impact of PRRSV infection is severe pneumonia. In the present study, we found that interleukin-17 (IL-17) was upregulated by PRRSV infection. Subsequently, we demonstrated that PI3K and p38MAPK signaling pathways were essential for PRRSV-induced IL-17 production as addition of phosphatidylinositol 3-kinase (PI3K) and p38MAPK inhibitors dramatically reduced IL-17 production. Furthermore, we show here that deleting the C/EBPβ and CREB binding motif in porcine IL-17 promoter abrogated its activation and that knockdown of C/EBPβ and CREB remarkably impaired PRRSV-induced IL-17 production, suggesting that IL-17 expression was dependent on C/EBPβ and CREB. More specifically, we demonstrate that PRRSV nonstructural protein 11 (nsp11) induced IL-17 production, which was also dependent on PI3K-p38MAPK-C/EBPβ/CREB pathways. We then show that Ser74 and Phe76 amino acids were essential for nsp11 to induce IL-17 production and viral rescue. In addition, IRAK1 was required for nsp11 to activate PI3K and enhance IL-17 expression by interacting with each other. Importantly, we demonstrate that PI3K inhibitor significantly suppressed IL-17 production and lung inflammation caused by HP-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.