Activation of the PKR/eIF2 alpha signaling cascade inhibits replication of Newcastle disease virus

文献类型： 外文期刊

第一作者： Zhang, Shilei

作者： Zhang, Shilei;Sun, Yingjie;Chen, Hongjun;Zhan, Yuan;Yu, Shengqing;Qiu, Xusheng;Tan, Lei;Song, Cuiping;Ding, Chan;Dai, Yabin

作者机构：

关键词： Newcastle disease virus;dsRNA;PKR;eIF2 alpha;HeLa cells

期刊名称：VIROLOGY JOURNAL （ 影响因子：4.099； 五年影响因子：3.719 ）

ISSN： 1743-422X

年卷期： 2014 年 11 卷

页码：

收录情况： SCI

摘要： Background: Newcastle Disease virus (NDV) causes severe and economically significant disease in almost all birds. However, factors that affect NDV replication in host cells are poorly understood. NDV generates long double-stranded RNA (dsRNA) molecules during transcription of single-stranded genomic RNA. Protein kinase R (PKR) is activated by dsRNA. The aim of this study was to elucidate the role of PKR in NDV infection. Results: NDV infection led to the activation of dsRNA-dependent PKR and phosphorylation of its substrate, translation initiation factor eIF2 alpha, in a dose-dependent manner by either the lentogenic strain LaSota or a velogenic strain Herts/33. PKR activation coincided with the accumulation of dsRNA induced by NDV infection. PKR knockdown remarkably decreased eIF2 alpha phosphorylation as well as IFN-beta mRNA levels, leading to the augmentation of extracellular virus titer. Furthermore, siRNA knockdown or phosphorylation of eIF2 alpha or okadaic acid treatment significantly impaired NDV replication, indicating the critical role of the PKR/eIF2 alpha signaling cascade in NDV infection. Conclusion: PKR is activated by dsRNA generated by NDV infection and inhibits NDV replication by eIF2 alpha phosphorylation. This study provides insight into NDV-host interactions for the development of candidate antiviral strategies.

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