Ziaie Z, Kefalides N A
Connective Tissue Research Institute, University of Pennsylvania, Philadelphia.
Biochem Biophys Res Commun. 1989 May 15;160(3):1073-8. doi: 10.1016/s0006-291x(89)80112-3.
In previous studies we have shown that herpes simplex virus type 1 (HSV-1) infection suppresses host-cell protein synthesis in human endothelial cells (EC). It has been demonstrated that lithium salts prevent viral replication in HSV-1 infected cells. In the present study, we have measured host-cell protein synthesis in HSV-1 infected EC in the presence or absence of 20 and 30 mM LiCl. Although LiCl restored synthesis of almost all host-cell proteins, [35S]methionine incorporation was most pronounced in thrombospondin and plasminogen activator inhibitor 1 and least in fibronectin and type IV collagen. LiCl was more effective at the higher concentration (30 mM) and when the compound was added to the EC culture at the time of infection rather than after adsorption of HSV-1. Synthesis of virus proteins continued in LiCl-treated EC but at a reduced rate. The data suggest that LiCl not only interferes with virus replication, but may also, to some extent, interfere with the virion-associated inhibition of host protein synthesis.
在先前的研究中，我们已经表明，单纯疱疹病毒1型（HSV-1）感染会抑制人内皮细胞（EC）中的宿主细胞蛋白质合成。已经证明，锂盐可阻止HSV-1感染细胞中的病毒复制。在本研究中，我们测定了在存在或不存在20 mM和30 mM LiCl的情况下，HSV-1感染的EC中的宿主细胞蛋白质合成。尽管LiCl恢复了几乎所有宿主细胞蛋白质的合成，但[35S]甲硫氨酸掺入在血小板反应蛋白和纤溶酶原激活物抑制剂1中最为明显，而在纤连蛋白和IV型胶原中最少。LiCl在较高浓度（30 mM）时更有效，并且当在感染时而非HSV-1吸附后将该化合物添加到EC培养物中时更有效。在LiCl处理的EC中病毒蛋白质的合成继续进行，但速率降低。数据表明，LiCl不仅干扰病毒复制，而且在一定程度上还可能干扰病毒体相关的宿主蛋白质合成抑制。
