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牛疱疹病毒1型的潜伏相关基因可抑制bICP0激活增殖性感染的能力。

The latency-related gene of bovine herpesvirus-1 can inhibit the ability of bICP0 to activate productive infection.

作者信息

Geiser Vicki, Inman Melissa, Zhang Yange, Jones Clinton

机构信息

School of Biological Sciences, University of Nebraska, Lincoln NE 68588, USA1.

Department of Veterinary and Biomedical Sciences, University of Nebraska, Lincoln, Fair Street at East Campus Loop, Lincoln, NE 68583-0905, USA2.

出版信息

J Gen Virol. 2002 Dec;83(Pt 12):2965-2971. doi: 10.1099/0022-1317-83-12-2965.

DOI:10.1099/0022-1317-83-12-2965
PMID:12466472
Abstract

Transfection of bovine cells with bovine herpesvirus-1 genomic DNA yields low levels of infectious virus. Cotransfection with the bICP0 gene enhances productive infection and virus yield because bICP0 can activate viral gene expression. Since the latency-related (LR) gene overlaps and is antisense to bICP0, the effects of LR gene products on productive infection were tested. The intact LR gene inhibited productive infection in a dose-dependent fashion but LR protein expression was not required. Further studies indicated that LR gene sequences near the 3' terminus of the LR RNA are necessary for inhibiting productive infection. When cotransfected with the bICP0 gene, the LR gene inhibited bICP0 RNA and protein expression in transiently transfected cells. Taken together, these results suggest that abundant LR RNA expression in sensory neurons is one factor that has the potential to inhibit productive infection and consequently promote the establishment and maintenance of latency.

摘要

用牛疱疹病毒1型基因组DNA转染牛细胞产生的感染性病毒水平较低。与bICP0基因共转染可增强生产性感染和病毒产量,因为bICP0可激活病毒基因表达。由于潜伏相关(LR)基因与bICP0重叠且为反义基因,因此测试了LR基因产物对生产性感染的影响。完整的LR基因以剂量依赖性方式抑制生产性感染,但不需要LR蛋白表达。进一步研究表明,LR RNA 3'末端附近的LR基因序列对于抑制生产性感染是必需的。当与bICP0基因共转染时,LR基因抑制瞬时转染细胞中bICP0 RNA和蛋白表达。综上所述,这些结果表明感觉神经元中丰富的LR RNA表达是有可能抑制生产性感染并因此促进潜伏建立和维持的一个因素。

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