Long non coding rna virus infection

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Membranes were then washed and incubated with horseradish peroxidase-conjugated anti-rabbit or anti-mouse secondary antibodies Biodragon, Beijing, China. The abundance of target genes was determined by qPCR. Finally, the protein bound to the beads was dissociated using elution buffer and analyzed by immunoblot assay.

Cells were then collected, and each single-cell clone was transferred into well plates following a limiting dilution method. Graphs were plotted and analyzed using GraphPad Prism version 6. We would like to thank Prof. CT and HC provided technical support. All authors read and approved the final manuscript. Publisher's Note. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Bojie Xu, Email: moc. Ruicheng Yang, Email: nc. Bo Yang, Email: moc. Liang Li, Email: nc. Jiaqi Chen, Email: moc. Jiyang Fu, Email: moc. Xinyi Qu, Email: moc. Dong Huo, Email: moc. Chen Tan, Email: nc. Huanchun Chen, Email: nc. Zhong Peng, Email: nc. Xiangru Wang, Email: nc. National Center for Biotechnology Information , U. Journal List Mol Brain v. Mol Brain.

Published online Jan 3. Author information Article notes Copyright and License information Disclaimer. Corresponding author. Received Sep 18; Accepted Dec The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material.

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Primers used for qPCR. Abstract Escherichia coli is the most common gram-negative pathogenic bacterium causing meningitis. Supplementary Information The online version contains supplementary material available at Introduction Bacterial meningitis is an important life-threatening infection of the central nervous system CNS , with high morbidity and mortality worldwide.

Results LncC11orf displayed differential expression during meningitic E. Open in a separate window. MgU promoted IRAK1 oligomerization and facilitated its auto-phosphorylation Although we have provided clues indicating that p65 is a key regulator of the mgUdependent inflammatory response, the details of the molecular mechanism by which mgU regulates p65 phosphorylation are unclear.

MgU promoted E. Supplementary Information Additional file 1: Table S1. Acknowledgements We would like to thank Prof. Availability of data and materials Data supporting the conclusions of this article are presented in this manuscript or Additional file 1. Declarations Ethics approval and consent to participate Not applicable.

Competing interests The authors declare that they have no competing interests. Footnotes Publisher's Note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Contributor Information Bojie Xu, Email: moc. References 1. Kim KS.

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It was found to modulate the infection of different viruses, including HCV, IAV and Semliki forest virus SFV , and also play important roles in several cancers, such as gastric cancer, glioma and renal cell carcinoma Xu et al. Interestingly, recent findings found that virus encoded lncRNAs may also participate in the antiviral response of IFN.

Except for functioning IFN antiviral response by regulating IFN induction and ISG expression, lncRNAs can also regulate viral infection and replication in an IFN-independent manner, impacting on the transcription of viral genes, the translocation of viral transcripts, the function of viral proteins, even host cell metabolism.

NEAT1 modulates the replication of different viruses by multiple mechanisms. It directly interacts with metabolic enzyme glutamic-oxaloacetic transaminease GOT2 in cytoplasm, resulting in increased catalytic activity of this enzyme, leading to enhanced production of key metabolites required for viral replication Kotzin et al.

IFN-mediated innate antiviral response is the first line of immune defense against viral infection. In the past decade, lncRNAs have been demonstrated to control fundamental biological processes at the epigenetic, transcription and post-transcriptional levels, and the deregulation of lncRNAs contributes to immune response, including IFN-mediated antiviral response. In this review, we summarized the deregulated lncRNAs upon viral infection, with special focus on the functions and underlying mechanisms of some important lncRNAs, and discussed their roles in the antiviral response of IFN.

TABLE 1. Except for impacting on IFN-mediated antiviral response, lncRNAs also modulate viral infection or replication by other mechanisms, such as regulating viral gene transcription, viral RNA translocation, viral protein function, and host cell metabolism. These indicate that different therapeutic strategies should be used to control different viruses. When host lncRNAs exert modulation on immune response, viruses have evolved to facilitate their survival and replication by regulating the expression of lncRNAs to influence different host pathways, suggesting the pivotal regulatory roles of lncRNAs in the interplay between host and viruses.

Until now, only a small part of lncRNAs have been identified and characterized to participate in the IFN antiviral response, while the vast majority of uncharacterized lncRNAs remain to be further explored.

More extensive studies are required to describe the precise profile of virus regulated lncRNAs and their functions in viral infection. Furthermore, the regulatory mechanisms of these lncRNAs by different viruses, as well as the underlying mechanisms of these lncRNAs in viral infection need to be fully elucidated.

The investigation of the interaction between lncRNA and the IFN antiviral response may not only deepen our understanding of antiviral response, but also provide novel applications for better prognosis and antiviral therapy. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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