ArticleScientific reports2019
The miRNA-targeted transcriptome of porcine alveolar macrophages upon infection with Porcine Reproductive and Respiratory Syndrome Virus.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- A New Long Noncoding RNA, MAHAT, Inhibits Replication of Porcine Reproductive and Respiratory Syndrome Virus by Recruiting DDX6 To Bind toJournal of virology · 2022Article
- MicroRNAs based regulation of cytokine regulating immune expressed genes and their transcription factors in COVID-19.Meta gene · 2022Article
- Comparative transcriptomics reveals small RNA composition and differential microRNA responses underlying interferon-mediated antiviral regulation in porcine alveolar macrophages.Frontiers in immunology · 2022Article
- Oral Epithelial Cells Distinguish betweenmSystems · 2021Article
- The Function of the PRRSV-Host Interactions and Their Effects on Viral Replication and Propagation in Antiviral Strategies.Vaccines · 2021Review
- Molecular and Cellular Mechanisms for PRRSV Pathogenesis and Host Response to Infection.Virus research · 2020Review
- The Encystment-Related MicroRNAs and Its Regulation Molecular Mechanism inInternational journal of molecular sciences · 2020Article
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Host miRNAs are known to modulate the cell response to virus infections. We characterized the miRNA-targeted transcriptome of porcine alveolar macrophages (PAMs) at early times after infection with a subtype 1.1 strain of PRRSV (Porcine Reproductive and Respiratory Syndrome Virus). We performed the immunoprecipitation of RISC (RNA-induced Silencing Complex) followed by microarray analysis of the RISC-bound miRNA targets (RIP-Chip) to evaluate the relative enrichment or depletion of expressed genes in RISC. The miRNA-mediated regulation occurred early after PRRSV infection and decreased fast (1,241 and 141 RISC-bound genes at 7 h and 10 h post-infection, respectively); it affected several cell functions with evidence of miRNA buffering of upregulated interferon-related genes. Eight miRNAs were highly enriched in RISC of both control and infected cells with no evidence of differential expression. Although miR-335-5p was the miRNA with most predicted targets among enriched RISC-bound genes, no effects on surface markers, cytokine expression and PRRSV replication were detected upon miR-335-5p mimics of primary PAMs. Our results do not point to specific miRNA-driven mechanisms regulating the early response to infection with this PRRSV 1.1 strain and indicate that the miRNome expressed by steady-state PAMs reacts promptly to counterbalance PRRSV infection by a pervasive modulation of host functions.
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