Roles of lncRNAs in influenza virus infection

Recent studies have identified host long noncoding RNAs (lncRNAs) as key regulators of host-virus interactions during viral infection. The influenza A virus (IAV) remains a serious threat to public health and economic stability. It is well known that thousands of lncRNAs are differentially expressed...

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Bibliographic Details
Published inEmerging microbes & infections Vol. 9; no. 1; pp. 1407 - 1414
Main Authors Wang, Jing, Cen, Shan
Format Journal Article
LanguageEnglish
Published United States Taylor & Francis 01.01.2020
Taylor & Francis Ltd
Taylor & Francis Group
Subjects
Animals
host immune response
Host-Pathogen Interactions
Humans
Infections
Influenza
Influenza A virus - genetics
Influenza A virus - physiology
influenza virus
Influenza, Human - genetics
Influenza, Human - metabolism
Influenza, Human - virology
LncRNAs
Review
RNA, Long Noncoding - genetics
RNA, Long Noncoding - metabolism
Viral infections
virus infection
Virus Replication
virus-host interaction
virus-host interaction
influenza virus
host immune response
LncRNAs
virus infection
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Summary:Recent studies have identified host long noncoding RNAs (lncRNAs) as key regulators of host-virus interactions during viral infection. The influenza A virus (IAV) remains a serious threat to public health and economic stability. It is well known that thousands of lncRNAs are differentially expressed upon IAV infection, some of which regulate IAV infection by modulating the host innate immune response, affecting cellular metabolism, or directly interacting with viral proteins. Some of these lncRNAs appear to be required for IAV infection, but the molecular mechanisms are not completely elucidated. In this review, we summarize the roles of host lncRNAs in regulating IAV infection and provide an overview of the lncRNA-mediated regulatory network. The goal of this review is to stimulate further research on the function of both well-established and newly discovered lncRNAs in IAV infection.
Bibliography:Abbreviations: CTL, cytotoxic T lymphocyte; EGOT, eosinophil granule ontogeny transcript; GOT2, glutamic-oxaloacetic transaminase; hnPNP U, heterogeneous nuclear ribonuclear protein U; IAV, influenza A virus; IFITM, interferon-induced transmembrane protein; IFN, interferon; IFNAR, interferon-α/β receptor; IPAN, influenza virus PB1-associated noncoding RNA; IRF, interferon regulatory factor; ISG, IFN-stimulated gene; ISR, interferon-stimulated lncRNA; ISRE, interferon-sensitive response element; IVPRIE, inhibiting IAV replication by promoting IFN and ISGs expression; JAK-STAT, Janus kinase-signal transducer and activator of transcription; lncRNA, long non-coding RNA; lncBST2/BISPR, BST2 IFN-stimulated positive regulator; MDA5, melanoma differentiation-associated gene 5; MxA, Myxovirus resistance protein 1; NEAT1, nuclear enriched abundant transcript 1; NRAV, negative regulator of anti-viral; OAS-RNase L, 2′-5′-oligoadenylate synthetase-ribonuclease L; PAMP, pathogen-associated molecular pattern; PB1, polymerase basic protein 1; PA, polymerase acidic protein; PAAN, PA-associated noncoding RNA; PKR protein kinase R; PRR, pattern recognition receptor; PTP1B, protein tyrosine phosphatase 1B; RIG-I, retinoic acid-inducible gene 1; SFPQ/PSF, splicing factor proline/glutamine-rich; TLR, toll-like receptor; TRIM, tripartite motif-containing; VIN, virus-inducible lincRNA; ZAP, zinc-finger antiviral protein
ISSN:2222-1751
2222-1751
DOI:10.1080/22221751.2020.1778429