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SARS-CoV-2 rORF3, a novel microprotein, impairs interferon-β production by targeting RanBP2 to inhibit p65 nuclear import

文献类型： 外文期刊

作者： Yucong Huang;Jing Jiang;Qingting Xiao;Yajie Wang;Gulinaziya Abulaike;Ayinuer Maimaiti;Pan Gong;Xiaohuang Lin;Fangfang Li;Xueping Zhou;Alexander F. Palazzo;Qingtang Shen

作者机构：

关键词： Innate immunity;Microprotein;p65;RanBP2;rORF3;Severe acute respiratory syndrome coronavirus 2

期刊名称： International Journal of Biological Macromolecules

ISSN： 0141-8130

年卷期： 2026 年 344 卷

页码：

收录情况： SCIE（2025版） ; ; EI（2025版）

摘要： Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of the coronavirus disease 2019 (COVID-19). SARS-CoV-2 encodes various proteins to evade host innate immunity. rORF3 is a novel microprotein encoded by the negative-strand RNA (-RNA) of SARS-CoV-2 that antagonizes type I interferon (IFN-I) production. However, the molecular mechanism by which SARS-CoV-2 rORF3 suppresses IFN-I production remains elusive. Here we report rORF3 interacts with a nucleoporin Ran-Binding Protein 2 (RanBP2), and suppresses IFN-β production and promotes viral infection in a RanBP2-dependent manner. Specifically, we found RanBP2 inhibits the RIG-I-like receptor (RLR)-mediated signaling by targeting p65 and suppressing the nuclear translocation of p65. rORF3 targets RanBP2 and impedes the nuclear translocation of p65 upon tumor necrosis factor-alpha (TNF-α) stimulation, thereby antagonizing IFN-β production. Our findings not only reveal a novel function of RanBP2 in regulating RLR signaling but also provide insights into a new mechanism of the innate immune evasion by SARS-CoV-2.

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