Retinol binding protein 4 restricts PCV2 replication via selective autophagy degradation of viral ORF1 protein

文献类型： 外文期刊

第一作者： Han, Qingbing

作者： Han, Qingbing;Zhao, Hejiao;Chen, Meng;Xue, Wenshuo;Shang, Yingli;Han, Qingbing;Zhao, Hejiao;Chen, Meng;Xue, Wenshuo;Shang, Yingli;Li, Jun;Sun, Lei;Shang, Yingli

作者机构：

期刊名称：COMMUNICATIONS BIOLOGY （ 影响因子：5.1； 五年影响因子：5.8 ）

ISSN：

年卷期： 2024 年 7 卷 1 期

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收录情况： SCI

摘要： Autophagy is a highly conserved degradative process that has been linked to various functions, including defending host cells against pathogens. Although the involvement of autophagy in porcine circovirus 2 (PCV2) infection has become apparent, it remains unclear whether selective autophagy plays a critical role in PCV2 restriction. Here we show that retinol-binding protein 4 (RBP4), an adipokine for retinol carrier, initiates the autophagic degradation of PCV2 ORF1 protein. PCV2 infection increases RBP4 protein levels through MAPK-eIF4E axis in living cells. Ectopic expression of RBP4 or recombinant RBP4 treatment promotes the degradation of ORF1 protein. Mechanistically, RBP4 activates TRAF6 to induce K63-linked ubiquitination of ORF1, leading to SQSTM1/p62-mediated selective autophagy for degradation. Consequently, RBP4 deficiency increases viral loads and exacerbates the pathogenicity of PCV2 in vivo. Collectively, these results identify RBP4 as a key host restriction factor of PCV2 and reveal a previously undescribed antiviral mechanism against PCV2 in infected cells. Retinol binding protein 4 activates TRAF6 to induce K63-linked ubiquitination and degradation of PCV2 ORF1 protein through SQSTM1/p62-mediated selective autophagy to restrict PCV2 replication.

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