Ebola virus replication is regulated by the phosphorylation of viral protein VP35

文献类型： 外文期刊

第一作者： Zhu, Lin

作者： Zhu, Lin;Xia, Xianzhu;Zhu, Lin;Gao, Ting;Yang, Weihong;Liu, Yaoning;Liu, Xuan;Hu, Yong;Jin, Yanwen;Li, Ping;Cao, Cheng;Xia, Xianzhu;Xu, Ke;Zou, Gang;Zhao, Lei;Cao, Ruiyuan;Zhong, Wu

作者机构：

关键词： VP35; Phosphorylation; S187; Minigenome; EBOV replication

期刊名称：BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS （ 影响因子：3.575； 五年影响因子：3.381 ）

ISSN： 0006-291X

年卷期： 2020 年 521 卷 3 期

页码：

收录情况： SCI

摘要： Ebola virus (EBOV) is a zoonotic pathogen, the infection often results in severe, potentially fatal, systematic disease in human and nonhuman primates. VP35, an essential viral RNA-dependent RNA polymerase cofactor, is indispensable for Ebola viral replication and host innate immune escape. In this study, VP35 was demonstrated to be phosphorylated at Serine/Threonine by immunoblotting, and the major phosphorylation sites was S187, S205, T206, S208 and S317 as revealed by LC-MS/MS. By an EBOV minigenomic system, EBOV minigenome replication was shown to be significantly inhibited by the phosphorylation-defective mutant, VP35 S187A, but was potentiated by the phosphorylation mimic mutant VP35 S187D. Together, our findings demonstrate that EBOV VP35 is phosphorylated on multiple residues in host cells, especially on S187, which may contribute to efficient viral genomic replication and viral proliferation. (C) 2019 Published by Elsevier Inc.

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