Stromal Interaction Molecule 1 Promotes the Replication of vvIBDV by Mobilizing Ca2+ in the ER

文献类型： 外文期刊

第一作者： Yan, Nana

作者： Yan, Nana;Wang, Yongqiang;Chen, Zehua;Liu, Aijing;Li, Yue;Yang, Bo;Li, Kai;Qi, Xiaole;Gao, Yulong;Gao, Li;Liu, Changjun;Zhang, Yanping;Cui, Hongyu;Pan, Qing;Wang, Xiaomei;Wang, Xiaomei

作者机构：

关键词： vvIBDV; STIM1; Ca2+

期刊名称：VIRUSES-BASEL （ 影响因子：5.818； 五年影响因子：5.811 ）

ISSN：

年卷期： 2022 年 14 卷 7 期

页码：

收录情况： SCI

摘要： Infectious bursal disease virus (IBDV) is one of the main threats to the poultry industry worldwide. Very virulent IBDV (vvIBDV) is a fatal virus strain that causes heavy mortality in young chicken flocks. Ca2+ is one of the most universal and versatile signalling molecules and is involved in almost every aspect of cellular processes. Clinical examination showed that one of the characteristics of vvIBDV-infected chickens was severe metabolic disorders, and the chemical examination showed that their serum Ca2+ level decreased significantly. However, there are limited studies on how vvIBDV infection modulates the cellular Ca2+ level and the effect of Ca2+ level changes on vvIBDV replication. In our study, we found Ca2+ levels in the endoplasmic reticulum (ER) of vvIBDV-infected B cells were higher than that of mock-infected cells, and the expression level of stromal interaction molecule 1 (STIM1), an ER Ca2+ sensor, was significantly upregulated due to vvIBDV infection. The knock-down expression of STIM1 led to decreased Ca2+ level in the ER and suppressed vvIBDV replication, while the over-expressed STIM1 led to ER Ca2+ upregulation and promoted vvIBDV replication. We also showed that the inhibition of Ca2+-release-activated-Ca2+ (CRAC) channels could reduce vvIBDV infection by blocking Ca2+ from entering the ER. This study suggests a new mechanism that STIM1 promotes the replication of vvIBDV by mobilizing Ca2+ in the ER.

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