Wang X, Xie J, Xu X, Liang F, Ding M
College of Life Sciences, Peking University, Beijing.
Wei Sheng Wu Xue Bao. 1994 Oct;34(5):345-54.
Sindbis virus (SBV) infection mediated a rapid shutoff of host cellular gene expression (mRNA synthesis and protein synthesis); however the synthesis of cellular rRNA remained at the same level as the uninfected cells. Meanwhile a cellular protein P105 was shown to be enriched in the nuclear matrix. Actionmycin D treatment after virus infection resulted in an apparent reduce in the production of viral structural proteins and infectious virions. The results presented here not only demonstrated the complexity of SBV-mediated regulation of host gene expression, but also suggested SBV nonstructural protein nsP2 and capsid protein C were possibly involved in this process.
辛德毕斯病毒（SBV）感染介导宿主细胞基因表达（mRNA合成和蛋白质合成）的快速关闭；然而，细胞rRNA的合成水平与未感染细胞相同。同时，一种细胞蛋白P105在核基质中富集。病毒感染后用放线菌素D处理导致病毒结构蛋白和感染性病毒粒子的产生明显减少。这里呈现的结果不仅证明了SBV介导的宿主基因表达调控的复杂性，还表明SBV非结构蛋白nsP2和衣壳蛋白C可能参与了这一过程。
