Interferon-induced MXB protein restricts vimentin-dependent viral infection

作者：Dongrong Yi, Ni An, Quanjie Li, Qian Liu, Huihan Shao, Rui Zhou, Jing Wang, Yongxin Zhang, Ling Ma, Fei Guo, Xiaoyu Li, Zhenlong Liu, Shan Cen · 发表于：Acta Pharmaceutica Sinica B · 年份：2024 · DOI：10.1016/j.apsb.2024.03.029 · 被引用次数：7 · 研究领域：interferon and immune responses、Herpesvirus Infections and Treatments、RNA regulation and disease

Type I interferon (IFN) inhibits a wide spectrum of viruses through stimulating the expression of antiviral proteins. As an IFN-induced protein, myxovirus resistance B (MXB) protein was reported to inhibit multiple highly pathogenic human viruses. It remains to be determined whether MXB employs a common mechanism to restrict different viruses. Here, we find that IFN alters the subcellular localization of hundreds of host proteins, and this IFN effect is partially lost upon MXB depletion. The results of our mechanistic study reveal that MXB recognizes vimentin (VIM) and recruits protein kinase B (AKT) to phosphorylate VIM at amino acid S38, which leads to reorganization of the VIM network and impairment of intracellular trafficking of virus protein complexes, hence causing a restriction of virus infection. These results highlight a new function of MXB in modulating VIM-mediated trafficking, which may lead towards a novel broad-spectrum antiviral strategy to control a large group of viruses that depend on VIM for successful replication.