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

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...

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Veröffentlicht in:Biotechnology and applied biochemistry 2020-05, Vol.67 (3), p.396-403, Article bab.1882
Hauptverfasser: Qiu, Yongle, Geng, Xixue, Ban, Jiandong, Liu, Yuanhang
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Sprache:eng
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Zusammenfassung: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.
ISSN:0885-4513
1470-8744
DOI:10.1002/bab.1882