Marcovistz R, Ermine A, Tsiang H
Microbiologica. 1983 Oct;6(4):293-304.
The protein synthesis of VSV infected CNS of mice was analysed by SDS-PAGE. Cellular and viral protein synthesis in the CNS were also compared to VSV infected neuroblastoma cells (clone NS 20) and fibroblasts (BHK21). Inhibition of host protein synthesis was observed in the three systems tested. However, this inhibition was shown to occur faster in neuroblastoma cells than in BHK cells, whereas it proceeded progressively in the brain. Thus the shut off of host cell protein synthesis by VSV seems to be a general phenomenon that occurs in vivo as well as in vitro. VSV protein from the CNS, or from neuroblastoma cells and fibroblasts were found to migrate similarly in SDS-PAGE. The viral L protein synthesis was found to be particularly active in the CNS, with respect to that observed in NS20 and BHK cells. The viral glycoprotein failed to be detected in the VSV infected mouse brain in our experimental conditions. The results show that VSV infection in vivo occurs with some difference with that of non neuronal cells, and that in vivo studies suggest the existence of cellular modulation that should be taken in account in the pathogenesis of this rhabdovirus.
通过SDS - PAGE分析了感染水疱性口炎病毒(VSV)的小鼠中枢神经系统(CNS)中的蛋白质合成。还将CNS中的细胞和病毒蛋白质合成与感染VSV的神经母细胞瘤细胞(克隆NS 20)和成纤维细胞(BHK21)进行了比较。在所测试的三个系统中均观察到宿主蛋白质合成受到抑制。然而,这种抑制在神经母细胞瘤细胞中比在BHK细胞中出现得更快,而在脑中则是逐渐发生的。因此,VSV对宿主细胞蛋白质合成的阻断似乎是一种在体内和体外都会发生的普遍现象。来自CNS、神经母细胞瘤细胞和成纤维细胞的VSV蛋白在SDS - PAGE中迁移情况相似。相对于在NS20和BHK细胞中观察到的情况,病毒L蛋白合成在CNS中特别活跃。在我们的实验条件下,在感染VSV的小鼠脑中未检测到病毒糖蛋白。结果表明,VSV在体内的感染与非神经元细胞的感染存在一些差异,并且体内研究表明存在细胞调节作用,这在这种弹状病毒的发病机制中应予以考虑。