LITHIUM-CHLORIDE RESTORES HOST PROTEIN-SYNTHESIS IN HERPES-SIMPLEX VIRUS-INFECTED ENDOTHELIAL-CELLS
LITHIUM-CHLORIDE RESTORES HOST PROTEIN-SYNTHESIS IN HERPES-SIMPLEX VIRUS-INFECTED ENDOTHELIAL-CELLS
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DOI：
10.1016/s0006-291x(89)80112-3
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发表时间：
1989-05-15
影响因子：
3.1
通讯作者：
KEFALIDES, NA
中科院分区：
文献类型：
--
作者：
ZIAIE, Z;KEFALIDES, NA
在以前的研究中，我们已经证明单纯疱疹病毒1型(HSV-1)感染会抑制人内皮细胞(EC)宿主细胞蛋白质的合成。已经证明，锂盐可以防止HSV-1感染细胞中的病毒复制。在本研究中，我们测定了在20 mM和30 mM LiCl存在或不存在的情况下，HSV-1感染EC的宿主细胞蛋白质合成。虽然LiCl恢复了几乎所有宿主细胞蛋白的合成，但[35S]蛋氨酸的掺入在凝血酶反应蛋白和纤溶酶原激活物抑制物1中最明显，在纤维连接蛋白和IV型胶原中最少。在较高浓度下(30 MM)，当该化合物在感染时加入EC培养时比在HSV-1吸附后加入EC培养时更有效。在经LiCl处理的EC中，病毒蛋白的合成仍在继续，但速度有所降低。这些数据表明，LiCl不仅干扰病毒复制，而且在一定程度上还可能干扰病毒粒子对宿主蛋白质合成的抑制。
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.