MicroRNA‐218 inhibits type I interferon production and facilitates virus immune evasion via targeting RIG‐I

• Published in: Biotechnology and applied biochemistry Vol. 67; no. 3; pp. 396 - 403
• Main Authors: Qiu, Yongle, Geng, Xixue, Ban, Jiandong, Liu, Yuanhang
• Format: Journal Article
• Language: English
• Published: United States Wiley Subscription Services, Inc 01-05-2020
• Subjects: Animals; Antigens; Antiviral Agents - immunology; Antiviral Agents - pharmacology; Cells, Cultured; DEAD Box Protein 58 - antagonists & inhibitors; DEAD Box Protein 58 - immunology; Immune evasion; Immune Evasion - drug effects; Immune Evasion - immunology; Immune system; Infections; Interferon; Interferon Type I - antagonists & inhibitors; Interferon Type I - biosynthesis; Macrophages; Macrophages - drug effects; Macrophages - immunology; Macrophages - virology; Male; Mice; Mice, Inbred C57BL; Microbial Sensitivity Tests; microRNA; MicroRNAs; MicroRNAs - genetics; MicroRNAs - immunology; miRNA; Retinoic acid; Ribonucleic acid; RIG‐I; RNA; Signaling; Vesiculovirus - drug effects; viral infection; Viral infections; Viruses; RIG-I; microRNA; macrophages; viral infection
• ISSN: 0885-4513; 1470-8744
• DOI: 10.1002/bab.1882

The host protective immunity against viral infection requires the effective detection of viral antigens and the subsequent production of type I interferons (IFNs) by host immune cells. Retinoic acid‐inducible gene I (RIG‐I) is the crucial signaling element responsible for sensing viral RNA component and initiating the downstream antiviral signaling pathways, leading to the production of type I IFNs. In this work, we identified microRNA‐218 (miR‐218) as a new virus‐induced miRNA that dampens the expression of RIG‐I in mouse and human macrophages, leading to the impaired production of type I IFNs. Interfering miR‐218 expression rescued RIG‐I‐mediated antiviral signaling and thus protected macrophages from viral infection. Hence, our results provide new understanding of miRNA‐mediated viral immune evasion and may be potentially useful for the treatment of viral infection in the future.
Macrophage infection by RNA virus leads to the upregulation of miR‐218, which targets and downregulates the expression of RIG‐I, leading to the impaired production of type I interferons. Hence, miR‐218 serves as a new pathogenic microRNA that contributes to viral immune evasion.