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鉴定和表征由新加坡石斑鱼虹彩病毒编码的肿瘤坏死因子受体样蛋白。

Identification and characterization of a tumor necrosis factor receptor like protein encoded by Singapore grouper iridovirus.

机构信息

Key Laboratory of Tropical Marine Bio-resources and Ecology, South China Sea Institute of Oceanology, Chinese Academy of Sciences, 164 West Xingang Road, Guangzhou 510301, China.

出版信息

Virus Res. 2013 Dec 26;178(2):340-8. doi: 10.1016/j.virusres.2013.09.023. Epub 2013 Sep 23.

DOI:10.1016/j.virusres.2013.09.023
PMID:24070984
Abstract

Virus encoded tumor necrosis factor receptors (TNFRs) have been demonstrated to facilitate virus to escape from apoptosis or other host immune response for viral replication. Singapore grouper iridovirus (SGIV), a large DNA virus which belongs to genus Ranavirus, is a major pathogen resulting in heavy economic losses to grouper aquaculture. Here, SGIV ORF096 (VP96) encoding a putative homolog of TNFR was identified and characterized. Multiple sequence alignment indicated that SGIV-VP96 contained two extracellular cysteine-rich domains (CRDs) with conserved four or six cysteine residues, but lacked the transmembrane domain at the C-terminus. SGIV-VP96 was identified as an early (E) gene and localized in the cytoplasm in transfected or infected cells. Overexpression of SGIV-VP96 in vitro enhanced cell proliferation, and improved cell survival against SGIV infection. Furthermore, virus infection induced apoptosis and caspase-3 activity were inhibited in SGIV-VP96 expressing FHM cells compared to the control cells. Taken together, our results suggested that SGIV might utilize virus encoded TNFR like genes to modulate the host apoptotic response for effective virus replication.

摘要

病毒编码的肿瘤坏死因子受体(TNFR)已被证明可促进病毒逃避细胞凋亡或其他宿主免疫反应,从而实现病毒复制。新加坡石斑鱼虹彩病毒(SGIV)是一种大型 DNA 病毒,属于 Ranavirus 属,是导致石斑鱼养殖业严重经济损失的主要病原体。在此,鉴定并表征了编码 TNFR 假定同源物的 SGIV ORF096(VP96)。多重序列比对表明,SGIV-VP96 包含两个具有保守的四个或六个半胱氨酸残基的细胞外富含半胱氨酸结构域(CRD),但在 C 末端缺乏跨膜结构域。SGIV-VP96 被鉴定为早期(E)基因,在转染或感染的细胞中定位于细胞质中。体外过表达 SGIV-VP96 可增强细胞增殖,并提高细胞对 SGIV 感染的存活率。此外,与对照细胞相比,在表达 SGIV-VP96 的 FHM 细胞中,病毒感染诱导的细胞凋亡和 caspase-3 活性受到抑制。总之,我们的结果表明,SGIV 可能利用病毒编码的 TNFR 样基因来调节宿主的细胞凋亡反应,以实现有效的病毒复制。

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