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      Genome-wide analysis of long noncoding RNA profiling in PRRSV-infected PAM cells by RNA sequencing

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          Abstract

          Porcine reproductive and respiratory syndrome (PRRS) is a major threat to the global swine industry and causes tremendous economic losses. Its causative agent, porcine reproductive and respiratory syndrome virus (PRRSV), primarily infects immune cells, such as porcine alveolar macrophages and dendritic cells. PRRSV infection results in immune suppression, antibody-dependent enhancement, and persistent infection. Highly pathogenic strains in China cause high fever and severe inflammatory responses in the lungs. However, the pathogenesis of PRRSV is still not fully understood. In this study, we analysed the long noncoding RNA (lncRNA) and mRNA expression profiles of the HP-PRRSV GSWW15 and the North American strain FL-12 in infected porcine alveolar macrophages (PAMs) at 12 and 24 hours post-infection. We predicted 12,867 novel lncRNAs, 299 of which were differentially expressed after viral infection. The Gene Ontology (GO) and Kyoto Encyclopaedia of Genes and Genomes (KEGG) analyses of the genes adjacent to lncRNAs showed that they were enriched in pathways related to viral infection and immune response, indicating that lncRNAs might play regulatory roles in virus-host interactions. Our study provided information about lncRNAs in the porcine immune system and offers new insights into the pathogenic mechanism of PRRSV infection and novel antiviral therapy development.

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          Most cited references31

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          The evolution of lncRNA repertoires and expression patterns in tetrapods.

          Only a very small fraction of long noncoding RNAs (lncRNAs) are well characterized. The evolutionary history of lncRNAs can provide insights into their functionality, but the absence of lncRNA annotations in non-model organisms has precluded comparative analyses. Here we present a large-scale evolutionary study of lncRNA repertoires and expression patterns, in 11 tetrapod species. We identify approximately 11,000 primate-specific lncRNAs and 2,500 highly conserved lncRNAs, including approximately 400 genes that are likely to have originated more than 300 million years ago. We find that lncRNAs, in particular ancient ones, are in general actively regulated and may function predominantly in embryonic development. Most lncRNAs evolve rapidly in terms of sequence and expression levels, but tissue specificities are often conserved. We compared expression patterns of homologous lncRNA and protein-coding families across tetrapods to reconstruct an evolutionarily conserved co-expression network. This network suggests potential functions for lncRNAs in fundamental processes such as spermatogenesis and synaptic transmission, but also in more specific mechanisms such as placenta development through microRNA production.
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            Long intergenic noncoding RNAs: new links in cancer progression.

            The process of cancer metastasis involves a series of sequential and complex steps. Here we give a perspective on recent results regarding noncoding transcription in cancer progression, focusing on the emerging role of long intergenic noncoding RNAs (lincRNAs). LincRNAs target chromatin modification complexes or RNA-binding proteins to alter gene expression programs. Similarly to miRNAs, lincRNAs exhibit distinct gene expression patterns in primary tumors and metastases. We discuss how lincRNAs can be used for cancer diagnosis and prognosis and serve as potential therapeutic targets. © 2011 AACR.
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              NRAV, a Long Noncoding RNA, Modulates Antiviral Responses through Suppression of Interferon-Stimulated Gene Transcription

              Summary Long noncoding RNAs (lncRNAs) modulate various biological processes, but their role in host antiviral responses is largely unknown. Here we identify a lncRNA as a key regulator of antiviral innate immunity. Following from the observation that a lncRNA that we call negative regulator of antiviral response (NRAV) was dramatically downregulated during infection with several viruses, we ectopically expressed NRAV in human cells or transgenic mice and found that it significantly promotes influenza A virus (IAV) replication and virulence. Conversely, silencing NRAV suppressed IAV replication and virus production, suggesting that reduction of NRAV is part of the host antiviral innate immune response to virus infection. NRAV negatively regulates the initial transcription of multiple critical interferon-stimulated genes (ISGs), including IFITM3 and MxA, by affecting histone modification of these genes. Our results provide evidence for a lncRNA in modulating the antiviral interferon response.
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                Author and article information

                Contributors
                liuzaixincaas@163.com
                luzengjun@caas.cn
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                10 July 2017
                10 July 2017
                2017
                : 7
                : 4952
                Affiliations
                ISNI 0000 0001 0018 8988, GRID grid.454892.6, State Key Laboratory of Veterinary Etiological Biology, , Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, ; Lanzhou, 730046 China
                Article
                5279
                10.1038/s41598-017-05279-z
                5504012
                28694521
                12da6f65-3c75-4d1f-b968-8cd5508566c4
                © The Author(s) 2017

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 22 November 2016
                : 26 May 2017
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