2017年3月27日， 國際學術權威刊物自然出版集團旗下子刊《Nature Communications》雜誌上線上發表了浙江大學醫學院王青青教授課題組題為“E3 ligase FBXW7 is critical for RIG-I stabilization during antiviral responses”的研究論文。 研究發現在病毒感染過程中， FBXW7通過保持RIG-I的穩定性， 促進I型干擾素的產生， 從而抑制病毒的感染。 宋寅敬博士、來利華博士後和種振路博士共同第一作者， 王青青教師、劉楊副教授為共同通訊作者。
機體在遭遇病原微生物感染後， 天然免疫細胞通過模式識別受體， 識別病原微生物中一系列保守的病原分子模式， 觸發迅速的天然免疫反應抵抗病原微生物的入侵。 RIG-I能夠識別病毒中的dsRNA，
該研究揭示了FBXW7在抗病毒天然免疫中發揮著重要的調控功能， 可為深入認識天然免疫的調節機制提供新的觀點並可能為治療感染性疾病提供新的思路和理論依據。
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The Hippo pathway senses cellular conditions and regulates YAP/TAZ to control cellular and tissue homeostasis, while TBK1 is central for cytosolic nucleic acid sensing and antiviral defence. The correlation between cellular nutrient/physical status and host antiviral defence is interesting but not well understood. Here we find that YAP/TAZ act as natural inhibitors of TBK1 and are vital for antiviral physiology. Independent of transcriptional regulation and through the transactivation domain, YAP/TAZ associate directly with TBK1 and abolish virus-induced TBK1 activation, by preventing TBK1 Lys63-linked ubiquitylation and the binding of adaptors/substrates. Accordingly, YAP/TAZ deletion/depletion or cellular conditions inactivating YAP/TAZ through Lats1/2 kinases relieve TBK1 suppression and boost antiviral responses, wheras expression of the transcriptionally inactive YAP dampens cytosolic RNA/DNAsensing and weakens the antiviral defence in cells and zebrafish. Thus, we describe a function of YAP/TAZ and the Hippo pathway in innate immunity, by linking cellular nutrient/physical status to antiviral host defence.