Legrand C, Rommelaere J, Caillet-Fauquet P
Département de Biologie Moléculaire, Faculté des Sciences, Université Libre de Bruxelles, Rhode St. Gen ese, Belgium.
Virology. 1993 Jul;195(1):149-55. doi: 10.1006/viro.1993.1355.
The parvovirus-encoded nonstructural (NS) proteins have been implicated in the cytopathogenicity of these agents. Although protein NS-1 of minute virus of mice (MVM) has been shown to be toxic, little is known about the role of NS-2 in this process. In order to determine the contribution of NS-1 and NS-2 to cytotoxicity, we took advantage of an expression system controlled by the mouse mammary tumor virus promoter which responds to glucocorticoid stimulation and which controls the expression of both MVM(p) NS proteins. Different mutations were introduced in NS genes so as to affect the NS-1 or NS-2 protein. Neoplastic human cell lines expressing only NS-1 protein after induction by dexamethasone undergo a smaller lethality compared to lines expressing both wild-type proteins. Mutations that were introduced in NS-1 coding sequence and did not affect NS-2 were found to drastically suppress the cytotoxic effect. It is concluded that the NS-2 protein has little cytotoxic activity by itself but is required for the full expression of the viral cytopathic effect on transformed human cells. Furthermore these results lead us to suggest that the NS-2 cytotoxic domain is localized in the amino-terminal portion of the protein.
细小病毒编码的非结构(NS)蛋白与这些病原体的细胞致病性有关。尽管小鼠微小病毒(MVM)的NS-1蛋白已被证明具有毒性,但关于NS-2在此过程中的作用却知之甚少。为了确定NS-1和NS-2对细胞毒性的贡献,我们利用了一个由小鼠乳腺肿瘤病毒启动子控制的表达系统,该启动子对糖皮质激素刺激有反应,并控制MVM(p)NS蛋白的表达。在NS基因中引入了不同的突变,以影响NS-1或NS-2蛋白。与表达两种野生型蛋白的细胞系相比,地塞米松诱导后仅表达NS-1蛋白的肿瘤性人类细胞系的致死率较低。在NS-1编码序列中引入且不影响NS-2的突变被发现可显著抑制细胞毒性作用。结论是,NS-2蛋白本身几乎没有细胞毒性活性,但对于病毒对转化人类细胞的细胞病变效应的充分表达是必需的。此外,这些结果使我们认为NS-2细胞毒性结构域位于该蛋白的氨基末端部分。