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MG-132 降低牛疱疹病毒-1 感染中的病毒释放。

MG-132 reduces virus release in Bovine herpesvirus-1 infection.

机构信息

Istituto Zooprofilattico Sperimentale del Mezzogiorno, Portici, 80055, Naples, Italy.

Department of Veterinary Medicine and Animal Production, University of Naples Federico II, 80137, Naples, Italy.

出版信息

Sci Rep. 2017 Oct 17;7(1):13306. doi: 10.1038/s41598-017-13717-1.

Abstract

Bovine herpesvirus 1 (BoHV-1) can provoke conjunctivitis, abortions and shipping fever. BoHV-1 infection can also cause immunosuppression and increased susceptibility to secondary bacterial infections, leading to pneumonia and occasionally to death. Herein, we investigated the influence of MG-132, a proteasome inhibitor, on BoHV-1 infection in bovine kidney (MDBK) cells. Infection of MDBK cells with BoHV-1 induces apoptotic cell death that enhances virus release. Whereas, MG-132 inhibited virus-induced apoptosis and stimulated autophagy. Protein expression of viral infected cell protein 0 (bICP0), which is constitutively expressed during infection and is able to stimulate Nuclear factor kappa B (NF-κB), was completely inhibited by MG-132. These results were accompanied by a significant delay in the NF-κB activation. Interestingly, the efficient virus release provoked by BoHV-1-induced apoptosis was significantly reduced by MG-132. Overall, this study suggests that MG-132, through the activation of autophagy, may limit BoHV-1 replication during productive infection, by providing an antiviral defense mechanism.

摘要

牛疱疹病毒 1(BoHV-1)可引起结膜炎、流产和运输热。BoHV-1 感染还可导致免疫抑制和继发细菌性感染的易感性增加,导致肺炎,偶尔导致死亡。在此,我们研究了蛋白酶体抑制剂 MG-132 对牛肾(MDBK)细胞中 BoHV-1 感染的影响。BoHV-1 感染 MDBK 细胞可诱导凋亡细胞死亡,从而促进病毒释放。然而,MG-132 抑制了病毒诱导的细胞凋亡并刺激了自噬。在感染过程中持续表达并能够刺激核因子 kappa B(NF-κB)的病毒感染细胞蛋白 0(bICP0)的蛋白表达被 MG-132 完全抑制。这些结果伴随着 NF-κB 激活的显著延迟。有趣的是,MG-132 显著降低了由 BoHV-1 诱导的细胞凋亡引起的有效病毒释放。总的来说,这项研究表明,MG-132 通过自噬的激活,可能通过提供抗病毒防御机制,在产感染期间限制 BoHV-1 的复制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1669/5645422/3e0995b978b0/41598_2017_13717_Fig1_HTML.jpg

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