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Updated: Aug 6, 2025

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
Published on: March 2, 2014
UBL7 enhances antiviral innate immunity by promoting Lys27-linked polyubiquitination of MAVS
Wei Jiang1, Xinyu Li2, Henan Xu1
1CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China.
Abstract:
RNA virus infection usually triggers a range of host immune responses, including the induction of proinflammatory cytokines, interferons, and interferon-stimulated genes (ISGs). Here, we report that UBL7, a ubiquitin-like protein, is upregulated during RNA virus infection and induced by type I interferon as an ISG. UBL7-deficient mice exhibit increased susceptibility to viral infection due to attenuated antiviral innate immunity. UBL7 enhances innate immune response to viral infection by promoting the K27-linked polyubiquitination of MAVS. UBL7 interacts with TRIM21, an E3 ubiquitin ligase of MAVS, and promotes the combination of TRIM21 with MAVS in a dose-dependent manner, facilitating the K27-linked polyubiquitination of MAVS and recruiting of TBK1 to enhance the IFN signaling pathway. Moreover, UBL7 has a broad-spectrum antiviral function as an immunomodulatory adaptor protein. Therefore, UBL7 positively regulates innate antiviral signaling and promotes positive feedback to enhance and amplify the antiviral response.
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