ArticleVeterinary microbiology2012
Porcine reproductive and respiratory syndrome virus activates the transcription of interferon alpha/beta (IFN-α/β) in monocyte-derived dendritic cells (Mo-DC).
Article in Veterinary microbiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 34 citations in OpenAlex.
- Article
- Porcine reproductive and respiratory syndrome virus nsp5 inhibits the activation of the Nrf2/HO-1 pathway by targeting p62 to antagonize its antiviral activity.Journal of virology · 2025Article
- Non-infectious immune complexes downregulate the production of interferons and tumor necrosis factor-α in primary porcine alveolar macrophagesFrontiers in veterinary science · 2024Article
- Genetic background influences pig responses to porcine reproductive and respiratory syndrome virus.Frontiers in veterinary science · 2023Review
- Evaluation of porcine GM-CSF during PRRSV infectionFrontiers in immunology · 2022Article
- Article
- Cellular Innate Immunity against PRRSV and Swine Influenza Viruses.Veterinary sciences · 2019Review
- Genotype 2 Strains of Porcine Reproductive and Respiratory Syndrome Virus Dysregulate Alveolar Macrophage Cytokine Production via the Unfolded Protein Response.Journal of virology · 2018Article
- Porcine reproductive and respiratory syndrome virus suppresses post-transcriptionally the protein expression of IFN-β by upregulating cellular microRNAs in porcine alveolar macrophagesExperimental and therapeutic medicine · 2018Article
- 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.Journal of virology · 2017Article
- Porcine epidemic diarrhea virus does not replicate in porcine monocyte-derived dendritic cells, but activates the transcription of type I interferon and chemokine.Veterinary microbiology · 2017Article
- Intranasal immunization of pigs with porcine reproductive and respiratory syndrome virus-like particles plus 2', 3'-cGAMP VacciGrade™ adjuvant exacerbates viremia after virus challenge.Virology journal · 2017Article
- Article
- Immunoregulatory effects triggered by immunobiotic Lactobacillus jensenii TL2937 strain involve efficient phagocytosis in porcine antigen presenting cells.BMC immunology · 2016Article
- Sensing of Porcine Reproductive and Respiratory Syndrome Virus-Infected Macrophages by Plasmacytoid Dendritic Cells.Frontiers in microbiology · 2016Article
- Article
- Innate and adaptive immunity against Porcine Reproductive and Respiratory Syndrome Virus.Veterinary immunology and immunopathology · 2015Review
- Current transcriptomics in pig immunity research.Mammalian genome : official journal of the International Mammalian Genome Society · 2015Review
- Modulation of innate immune signaling by nonstructural protein 1 (nsp1) in the family Arteriviridae.Virus research · 2014Review
- Porcine reproductive and respiratory syndrome (PRRS): an immune dysregulatory pandemic.Immunologic research · 2014Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Porcine reproductive and respiratory syndrome virus (PRRSV) is known to be a poor inducer of interferon alpha/beta (IFN-α/β), which may contribute to the delayed development of adaptive immunity and the resultant viral persistence. However, the exact mechanism by which PRRSV inhibits the induction of IFN-α/β during infection of its natural host cells remains less well defined. Here, we show that PRRSV efficiently activates the transcription of IFN-α/β in porcine monocyte-derived dendritic cells (Mo-DC) in a time-dependent and transient manner; and this effect is dependent on the activation of phosphatidylinositol 3-kinase (PI3K). Despite the abundant IFN-α transcripts detected in PRRSV-infected Mo-DC, little or no detectable IFN-α is found in the supernatants and cell lysates of PRRSV-infected Mo-DC, suggesting that PRRSV either blocks the translation of IFN-α or inhibits the RNA processing and transport. Furthermore, we observed that PRRSV infection significantly reduced the induction of IFN-α by Poly I:C treatment; and virus replication is essential to the effect since heat-inactivated PRRSV has no effect on IFN-α induction by Poly I:C. Overall, our data provide evidence for the possible role of PI3K in the activation of the transcription of IFN-α/β by PRRSV. We conclude that PRRSV inhibits the induction of IFN-α in Mo-DC by as yet undefined post-transcriptional mechanisms.
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Registered trials
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