Regulation of influenza virus infection by long non-coding RNAs
Regulation of influenza virus infection by long non-coding RNAs
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DOI：
10.1016/j.virusres.2015.08.008
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发表时间：
2016-01-02
期刊：
影响因子：
5
通讯作者：
Ortin, Juan
中科院分区：
文献类型：
--
作者：
Landeras-Bueno, Sara;Ortin, Juan
甲型流感病毒引起呼吸道疾病的年度流行和偶尔大流行，对人类健康和经济产生重要影响。为了建立生产性感染，流感病毒与细胞因子相互作用以促进其自身复制并抑制抗病毒细胞反应。尽管大多数病毒-宿主相互作用的研究集中在细胞蛋白因子上，但大多数人类转录组包含非编码RNA，如miRNA和lncRNA。后者是许多细胞过程中的关键细胞调节因子，包括转录和转录后调节。流感病毒感染诱导数百种潜在的lncRNA的差异表达，其中一些与细胞激活的抗病毒途径有关，而另一些则可能因感染而失调，以允许有效的病毒增殖。虽然我们对细胞lncRNA在流感病毒复制和发病机制中的作用的认识仍处于起步阶段，但已经描述了几种lncRNA通过改变特定位点的组蛋白修饰、通过与特定转录因子相互作用或直接顺式刺激特定IFN诱导基因的表达来影响细胞对病毒的先天应答。此外，至少一种lncRNA似乎是以IFN-非依赖性方式进行病毒增殖所需的。(C)2015 Elsevier B. V.版权所有。
Influenza A viruses generate annual epidemics and occasional pandemics of respiratory disease with important consequences for human health and economy. To establish a productive infection, influenza viruses interact with cellular factors to favour their own replication and to suppress antiviral cell responses. Although most virus-host interaction studies have been centred on cell protein factors, most of the human transcriptome comprises non-coding RNAs, as miRNAs and lncRNAs. The latter are key cellular regulators in many cellular processes, including transcriptional and post-transcriptional regulation. Influenza virus infection induces the differential expression of hundreds of potential lncRNAs, some of which are related to the antiviral pathways activated by the cell while others may be deregulated by the infection to allow efficient virus multiplication. Although our knowledge on the role of cellular lncRNAs for influenza virus replication and pathogenesis is still at its infancy, several lncRNAs have been described to influence the cell innate response to the virus by altering the histone modification at specific sites, by interaction with specific transcription factors or directly stimulating in cis the expression of specific IFN-induced genes. In addition, at least one lncRNA appears to be required for virus multiplication in an IFN-independent way. (C) 2015 Elsevier B.V. All rights reserved.