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Cell Host Microbe. 2014 Nov 12;16(5):616-26. doi: 10.1016/j.chom.2014.10.001. Epub 2014 Nov 12.

NRAV, a long noncoding RNA, modulates antiviral responses through suppression of interferon-stimulated gene transcription.

Author information

1
CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China.
2
CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China; School of Life Sciences, Anhui University, Hefei 230601, China.
3
CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China; College of Animal Sciences, Fujian Agriculture and Forestry University, Fuzhou 350002, China.
4
College of Animal Sciences, Fujian Agriculture and Forestry University, Fuzhou 350002, China.
5
Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences & Comparative Medical Center, Beijing 100021, China.
6
Key Laboratory of Intelligent Information Processing, Institute of Computing Technology, Chinese Academy of Sciences, Beijing 100190, China.
7
Gene Therapy Program, Departments of Microbiology and Immunology, Medicine and Genetics, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA.
8
CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China; College of Animal Sciences, Fujian Agriculture and Forestry University, Fuzhou 350002, China. Electronic address: chenjl@im.ac.cn.

Abstract

Long noncoding RNAs (lncRNAs) modulate various biological processes, but their role in host antiviral responses is largely unknown. Here we identify a lncRNA as a key regulator of antiviral innate immunity. Following from the observation that a lncRNA that we call negative regulator of antiviral response (NRAV) was dramatically downregulated during infection with several viruses, we ectopically expressed NRAV in human cells or transgenic mice and found that it significantly promotes influenza A virus (IAV) replication and virulence. Conversely, silencing NRAV suppressed IAV replication and virus production, suggesting that reduction of NRAV is part of the host antiviral innate immune response to virus infection. NRAV negatively regulates the initial transcription of multiple critical interferon-stimulated genes (ISGs), including IFITM3 and MxA, by affecting histone modification of these genes. Our results provide evidence for a lncRNA in modulating the antiviral interferon response.

PMID:
25525793
DOI:
10.1016/j.chom.2014.10.001
[Indexed for MEDLINE]
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