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Proc Natl Acad Sci U S A. 2016 Sep 13;113(37):10388-93. doi: 10.1073/pnas.1525022113. Epub 2016 Aug 31.

Long noncoding RNA #32 contributes to antiviral responses by controlling interferon-stimulated gene expression.

Author information

1
Research Center for Hepatitis and Immunology, National Center for Global Health and Medicine, Ichikawa, Chiba 272-8516, Japan lbnishitsuji@hospk.ncgm.go.jp.
2
Research Center for Hepatitis and Immunology, National Center for Global Health and Medicine, Ichikawa, Chiba 272-8516, Japan.

Abstract

Despite the breadth of knowledge that exists regarding the function of long noncoding RNAs (lncRNAs) in biological phenomena, the role of lncRNAs in host antiviral responses is poorly understood. Here, we report that lncRNA#32 is associated with type I IFN signaling. The silencing of lncRNA#32 dramatically reduced the level of IFN-stimulated gene (ISG) expression, resulting in sensitivity to encephalomyocarditis virus (EMCV) infection. In contrast, the ectopic expression of lncRNA#32 significantly suppressed EMCV replication, suggesting that lncRNA#32 positively regulates the host antiviral response. We further demonstrated the suppressive function of lncRNA#32 in hepatitis B virus and hepatitis C virus infection. lncRNA#32 bound to activating transcription factor 2 (ATF2) and regulated ISG expression. Our results reveal a role for lncRNA#32 in host antiviral responses.

KEYWORDS:

ISG; innate immunity; interferon; lncRNA

PMID:
27582466
PMCID:
PMC5027408
DOI:
10.1073/pnas.1525022113
[Indexed for MEDLINE]
Free PMC Article

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