The C-type lectin homologue gene (EP153R) of African swine fever virus inhibits apoptosis both in virus infection and in heterologous expression
The C-type lectin homologue gene (EP153R) of African swine fever virus inhibits apoptosis both in virus infection and in heterologous expression
复制标题
DOI：
10.1016/j.virol.2004.05.019
复制
发表时间：
2004-08-15
期刊：
影响因子：
3.7
通讯作者：
Carrascosa, AL
中科院分区：
文献类型：
--
作者：
Hurtado, C;Granja, AG;Carrascosa, AL
非洲猪瘟病毒 (ASFV) 的开放阅读框 EP153R 编码一种非必需蛋白，该蛋白参与病毒感染细胞诱导的血细胞吸附过程。通过使用缺乏 EP153R 基因的病毒缺失突变体，我们在一些病毒敏感细胞中检测到与亲本 BA71V 毒株感染后获得的结果相比，caspase-3 水平和细胞死亡有所增加。 EP153R 基因在 Vero 或 COS 细胞中的瞬时和稳定表达都导致转染细胞系免受因病毒感染或外部刺激而诱导的细胞凋亡的部分保护。基因 EP153R 的存在导致 Vero 细胞培养物中细胞蛋白 p53 的反式激活活性降低，其中病毒感染或十字孢菌素处理诱导细胞凋亡。据我们所知，这是对具有抗凋亡特性的病毒 C 型凝集素的首次描述。 (C) 2004 Elsevier Inc. 保留所有权利。
The open reading frame EP153R of African swine fever virus (ASFV) encodes a nonessential protein that has been involved in the hemadsorption process induced in virus-infected cells. By the use of a virus deletion mutant lacking the EP153R gene, we have detected, in several virus-sensitive cells, increased levels of caspase-3 and cell death as compared with those obtained after infection with the parental BA71V strain. Both transient and stable expression of the EP153R gene in Vero or COS cells resulted in a partial protection of the transfected lines from the apoptosis induced in response to virus infection or external stimuli. The presence of gene EP153R resulted in a reduction of the transactivating activity of the cellular protein p53 in Vero cell cultures in which apoptosis was induced by virus infection or staurosporine treatment. This is to our knowledge the first description of a viral C-type lectin with anti-apoptotic properties. (C) 2004 Elsevier Inc. All rights reserved.