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牛疱疹病毒5型感染调节Bax/BCL-2比率。

Bovine herpesvirus type 5 infection regulates Bax/BCL-2 ratio.

作者信息

Garcia A F, Novais J B, Antello T F, Silva-Frade C, Ferrarezi M C, Flores E F, Cardoso T C

机构信息

Laboratório de Virologia Animal e Cultivo Celular, Faculdade de Medicina Veterinária, Universidade Estadual Paulista, Araçatuba, SP, Brasil.

出版信息

Genet Mol Res. 2013 Sep 23;12(3):3897-904. doi: 10.4238/2013.September.23.8.

DOI:10.4238/2013.September.23.8
PMID:24085451
Abstract

Bovine herpesvirus 5 (BoHV-5) is an α-herpesvirus that causes neurological disease in young cattle and is also occasionally involved in reproductive disorders. Although there have been many studies of the apoptotic pathways induced by viruses belonging to the family Herpesviridae, there is little information about the intrinsic programmed cell death pathway in host-BoHV-5 interactions. We found that BoHV-5 is able to replicate in both mesenchymal and epithelial cell lines, provoking cytopathology that is characterized by cellular swelling and cell fusion. Viral antigens were detected in infected cells by immunofluorescence assay at 48 to 96 h post-infection (p.i.). At 48 to 72 h p.i., anti-apoptotic BCL-2 antigens were found at higher levels than Bax antigens; the latter is considered a pro-apoptotic protein. Infected cells had increased BCL-2 phenotype cells from 48 to 96 h p.i., based on flow cytometric analysis. At 48 to 96 h p.i., Bax mRNA was not expressed in any of the infected cell monolayers. In contrast, BCL-2 mRNA was found at high levels at all p.i. in both types of cells. BoHV-5 replication apparently modulates BCL-2 expression and gene transcription, enhancing production of virus progeny.

摘要

牛疱疹病毒5型(BoHV-5)是一种α疱疹病毒,可导致幼龄牛出现神经疾病,偶尔也会引发生殖障碍。尽管对疱疹病毒科病毒诱导的凋亡途径已有许多研究,但关于宿主与BoHV-5相互作用中的内源性程序性细胞死亡途径的信息却很少。我们发现BoHV-5能够在间充质和上皮细胞系中复制,引发以细胞肿胀和细胞融合为特征的细胞病变。在感染后(p.i.)48至96小时通过免疫荧光测定法在感染细胞中检测到病毒抗原。在感染后48至72小时,抗凋亡BCL-2抗原的水平高于Bax抗原;后者被认为是一种促凋亡蛋白。基于流式细胞术分析,感染细胞在感染后48至96小时内具有增加的BCL-2表型细胞。在感染后48至96小时,任何感染的细胞单层中均未表达Bax mRNA。相反,在两种类型的细胞中,在所有感染时间点均发现高水平的BCL-2 mRNA。BoHV-5复制显然调节BCL-2表达和基因转录,从而增强病毒子代的产生。

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