Journal
THERANOSTICS
Volume 10, Issue 20, Pages 9407-9424Publisher
IVYSPRING INT PUBL
DOI: 10.7150/thno.48520
Keywords
long non-coding RNAs; RNA-binding proteins; innate antiviral responses; N-6-methyladenosine; TRIM family
Categories
Funding
- National Natural Science Foundation of China [81872908, 81573471]
- Science and Technology Program of Guangzhou, China [201604020178]
- Key Projects of Biological Industry Science AMP
- Technology of Guangzhou China [201300000060]
- Science AMP
- Technology Plan Program of Guangdong Province China [2012A080204003]
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The diseases caused by viruses posed a great challenge to human health, the development of which was driven by the imbalanced host immune response. Host innate immunity is an evolutionary old defense system that is critical for the elimination of the virus. The overactive innate immune response also leads to inflammatory autoimmune diseases, which require precise control of innate antiviral response for maintaining immune homeostasis. Mounting long non-coding RNAs (lncRNAs) transcribed from the mammalian genome are key regulators of innate antiviral response, functions of which greatly depend on their protein interactors, including classical RNA-binding proteins (RBPs) and the unconventional proteins without classical RNA binding domains. In particular, several emerging RBPs, such as m(6)A machinery components, TRIM family members, and even the DNA binding factors recognized traditionally, function in innate antiviral response. In this review, we highlight recent progress in the regulation of type I interferon signaling-based antiviral responses by IncRNAs and emerging RBPs as well as their mechanism of actions. We then posed the future perspective toward the role of lncRNA-RBP interaction networks in innate antiviral response and discussed the promising and challenges of lncRNA-based drug development as well as the technical bottleneck in studying lncRNA-protein interactions. Our review provides a comprehensive understanding of lncRNA and emerging RBPs in the innate antiviral immune response.
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