tetano
Editor, Senior Moderator
Virus Res. 2015 Aug 27. pii: S0168-1702(15)30040-X. doi: 10.1016/j.virusres.2015.08.008. [Epub ahead of print]
[h=1]Regulation of influenza virus infection by long non-coding RNAs.[/h] Landeras-Bueno S[SUP]1[/SUP], Ort?n J[SUP]2[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Influenza A viruses generate annual epidemics and occasional pandemics of respiratorydisease with important consequences for human health and economy. To establish a productiveinfection, influenza viruses interact with cellular factors to favour their own replication and tosuppress antiviral cell responses. Although most virus-host interaction studies have been centred oncell protein factors, most of the human transcriptome comprises non-coding RNAs, as miRNAs andlncRNAs. The latter are key cellular regulators in many cellular processes, including transcriptional andpost-transcriptional regulation. Influenza virus infection induces the differential expression ofhundreds of potential lncRNAs, some of which are related to the antiviral pathways activated by thecell while others may be deregulated by the infection to allow efficient virus multiplication. Althoughour knowledge on the role of cellular lncRNAs for influenza virus replication and pathogenesis is still atits infancy, several lncRNAs have been described to influence the cell innate response to the virus byaltering the histone modification at specific sites, by interaction with specific transcription factors ordirectly stimulating in cis the expression of specific IFN-induced genes. In addition, at least one lncRNAappears to be required for virus multiplication in an IFN-independent way.
Copyright ? 2015 Elsevier B.V. All rights reserved.
[h=4]KEYWORDS:[/h] IFN; influenza; lncRNAs
PMID: 26321158 [PubMed - as supplied by publisher]
[h=1]Regulation of influenza virus infection by long non-coding RNAs.[/h] Landeras-Bueno S[SUP]1[/SUP], Ort?n J[SUP]2[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Influenza A viruses generate annual epidemics and occasional pandemics of respiratorydisease with important consequences for human health and economy. To establish a productiveinfection, influenza viruses interact with cellular factors to favour their own replication and tosuppress antiviral cell responses. Although most virus-host interaction studies have been centred oncell protein factors, most of the human transcriptome comprises non-coding RNAs, as miRNAs andlncRNAs. The latter are key cellular regulators in many cellular processes, including transcriptional andpost-transcriptional regulation. Influenza virus infection induces the differential expression ofhundreds of potential lncRNAs, some of which are related to the antiviral pathways activated by thecell while others may be deregulated by the infection to allow efficient virus multiplication. Althoughour knowledge on the role of cellular lncRNAs for influenza virus replication and pathogenesis is still atits infancy, several lncRNAs have been described to influence the cell innate response to the virus byaltering the histone modification at specific sites, by interaction with specific transcription factors ordirectly stimulating in cis the expression of specific IFN-induced genes. In addition, at least one lncRNAappears to be required for virus multiplication in an IFN-independent way.
Copyright ? 2015 Elsevier B.V. All rights reserved.
[h=4]KEYWORDS:[/h] IFN; influenza; lncRNAs
PMID: 26321158 [PubMed - as supplied by publisher]