ADP-ribosylation factor 6 promotes infectious bursal disease virus replication by affecting the internalization process via clathrin

文献类型： 外文期刊

第一作者： Zhang, Xinxin

作者： Zhang, Xinxin;Gao, Pei;Wang, Li;Liu, Liu;Wang, Qiuxia;Xu, Zhiyong;Zhang, Yanhong;Yu, Yan;Ma, Jinyou;Zhang, Xinxin

作者机构：

关键词： ARF6; IBDV; Replication; Internalization; Clathrin

期刊名称：VETERINARY MICROBIOLOGY （ 影响因子：3.3； 五年影响因子：3.5 ）

ISSN： 0378-1135

年卷期： 2024 年 290 卷

页码：

收录情况： SCI

摘要： ADP-ribosylation factor 6 (ARF6) is a small G protein with extensive functions, including regulation of cellular membrane transport and viral infection. Infectious bursal disease (IBD) is caused by infectious bursal disease virus (IBDV), which mainly invades the bursa of Fabricius and causes low immunity in poultry. Our study demonstrated that IBDV infection could promote the expression of ARF6; however, the underlying mechanism remains unclear. Herein, the function of ARF6 in IBDV infection was explored, and it was revealed that viral replication was significantly promoted by ARF6 overexpression and hampered by siRNA-mediated inhibition of ARF6. Using two site mutants of ARF6 (ARF6-T27N and ARF6-Q67L), we found that IBDV replication was repressed by ARF6-T27N, indicating that ARF6 promotes IBDV replication. Further exploration of its mechanism revealed that ARF6 affects the copy number of IBDVs entering cells. A clathrin inhibitor (pitstop 2) impeded the early replication of IBDV, even when ARF6 was overexpressed. These results indicated that ARF6 promotes viral replication by affecting the internalization of IBDV, which may involve clathrin-dependent endocytosis. Our findings improve the understanding of the processes governing IBDV infection and provide insights into its prevention and control.

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