磷脂酰肌醇 3-激酶和 mTOR 的抑制剂但不是 Akt 增强了牛暂时热病毒的复制。

Inhibitors of phosphatidylinositol 3-kinase and mTOR but not Akt enhance replication of bovine ephemeral fever virus.

机构信息

Department of Veterinary Medicine, National Pingtung University of Science and Technology, Pingtung 912, Taiwan.

出版信息

Vet J. 2011 Jan;187(1):119-23. doi: 10.1016/j.tvjl.2009.11.003. Epub 2010 Jan 13.

DOI:10.1016/j.tvjl.2009.11.003

PMID:20074986

Abstract

Non-segmented, negative-sense RNA viruses (NNSVs) depend on Akt (protein kinase B) for efficient replication. Infection with bovine ephemeral fever virus (BEFV) increases Akt phosphorylation. This study examined the effect of inhibition of phosphatidylinositol 3-kinase (PI3K)-Akt signalling on BEFV replication, since PI3K is the major upstream regulator of Akt. Treatment of BEFV-infected cells with two specific PI3K inhibitors (wortmannin and LY294002) enhanced replication of BEFV when compared to the effects of Akt inhibitors III and IV. BEFV antagonised the effects of PI3K inhibitors on Akt dephosphorylation. Inhibition of mTOR by rapamycin also enhanced replication of BEFV. The results provide evidences that inhibition of PI3K and mTOR has positive effects on replication of BEFV.

摘要

非分段、负义 RNA 病毒 (NNSVs) 依赖 Akt（蛋白激酶 B）进行高效复制。感染牛暂时热病毒 (BEFV) 会增加 Akt 的磷酸化。本研究检测了抑制磷酸肌醇 3-激酶 (PI3K)-Akt 信号通路对 BEFV 复制的影响，因为 PI3K 是 Akt 的主要上游调节剂。与 Akt 抑制剂 III 和 IV 的作用相比，用两种特异性 PI3K 抑制剂（wortmannin 和 LY294002）处理 BEFV 感染的细胞会增强 BEFV 的复制。BEFV 拮抗了 PI3K 抑制剂对 Akt 去磷酸化的作用。雷帕霉素抑制 mTOR 也增强了 BEFV 的复制。结果提供了证据，表明抑制 PI3K 和 mTOR 对 BEFV 的复制有积极影响。