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病毒基因α 3 与宿主异质核核糖核蛋白 K 的相互作用调控细胞凋亡,促进牛暂时热病毒复制。

Cell apoptosis regulated by interaction between viral gene alpha 3 and host heterogeneous nuclear ribonucleoprotein K facilitates bovine ephemeral fever virus replication.

机构信息

Ruminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan 250014, China.

出版信息

Vet Microbiol. 2020 Jan;240:108510. doi: 10.1016/j.vetmic.2019.108510. Epub 2019 Nov 15.

Abstract

Bovine ephemeral fever virus (BEFV) is an arthropod-borne rhabdovirus and causes bovine ephemeral fever of cattle and water buffalo in worldwide. Previous studies have demonstrated that infection with BEFV leads to induction of host cellular apoptosis. However, the role of apoptosis in viral replication and the interaction between viral genes and host genes involved in the process of BEFV-induced apoptosis remains unclear. Herein we investigated the interaction between viral non-structural protein α3 and cellular heterogeneous nuclear ribonucleoprotein K (hnRNP K) in the BEFV-induced apoptosis and its role in virus replication. Overexpression of α3 gene activated caspase 3 and consequently cleaved PARP, ultimately lead to apoptosis. Moreover, virus titer of BHK-21 cells infected with BEFV and then treated respectively by the pan-caspase inhibitor (Z-VAD-FMK) and apoptosis inducer (CCCP) was determined, the results showed that apoptosis promoted viral replication. In addition, knockdown of hnRNP K gene promoted BEFV replication, whereas overexpression of hnRNP K gene had the opposite effects. More importantly, overexpression of hnRNP K inhibited virus-induced apoptosis. Subsequently, it was found that hnRNP K suppressed BEFV replication via degrading viral α3 gene and further inhibited apoptosis induced by α3 gene. Finally, the expression of hnRNP K protein was significantly down-regulated upon BEFV infection, and degradation of hnRNP K protein in BHK-21 cells infected with BEFV was mediated by viral activation of caspase 3. Taken together, these results suggest that apoptosis takes a pivotal role in BEFV replication, and interaction between viral α3 gene and host hnRNP K gene in BEFV-induced apoptosis facilitates BEFV replication.

摘要

牛暂时热病毒(BEFV)是一种节肢动物传播的弹状病毒,可引起全世界牛和水牛的牛暂时热。先前的研究表明,BEFV 感染会导致宿主细胞凋亡。然而,凋亡在病毒复制中的作用以及病毒基因与宿主基因之间的相互作用,涉及到 BEFV 诱导的凋亡过程仍不清楚。在此,我们研究了 BEFV 诱导的凋亡过程中病毒非结构蛋白α3与细胞异质核核糖核蛋白 K(hnRNP K)之间的相互作用及其在病毒复制中的作用。α3 基因的过表达激活了半胱天冬酶 3,进而切割了 PARP,最终导致了凋亡。此外,我们通过分别用泛半胱天冬酶抑制剂(Z-VAD-FMK)和凋亡诱导剂(CCCP)处理感染了 BEFV 的 BHK-21 细胞,测定了病毒滴度,结果表明凋亡促进了病毒复制。另外,hnRNP K 基因的敲低促进了 BEFV 的复制,而 hnRNP K 基因的过表达则产生了相反的效果。更重要的是,hnRNP K 的过表达抑制了病毒诱导的凋亡。随后发现,hnRNP K 通过降解病毒α3 基因抑制 BEFV 的复制,进而抑制了α3 基因诱导的凋亡。最后,在 BEFV 感染后,hnRNP K 蛋白的表达明显下调,并且在 BEFV 感染的 BHK-21 细胞中,hnRNP K 蛋白的降解是由病毒激活半胱天冬酶 3介导的。综上所述,这些结果表明凋亡在 BEFV 复制中起着关键作用,而 BEFV 诱导的凋亡中病毒α3 基因与宿主 hnRNP K 基因之间的相互作用促进了 BEFV 的复制。

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