水痘带状疱疹病毒（VZV）糖蛋白E的胰岛素降解酶结合结构域对细胞间传播和VZV感染性很重要，而糖蛋白I结合结构域对感染至关重要。

The insulin degrading enzyme binding domain of varicella-zoster virus (VZV) glycoprotein E is important for cell-to-cell spread and VZV infectivity, while a glycoprotein I binding domain is essential for infection.

作者信息

Ali Mir A, Li Qingxue, Fischer Elizabeth R, Cohen Jeffrey I

机构信息

Medical Virology Section, Laboratory of Clinical Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.

出版信息

Virology. 2009 Apr 10;386(2):270-9. doi: 10.1016/j.virol.2009.01.023. Epub 2009 Feb 23.

Varicella-zoster virus (VZV) glycoprotein E (gE) interacts with glycoprotein I and with insulin degrading enzyme (IDE), which is a receptor for the virus. We found that a VZV gE deletion mutant could only be grown in cells expressing gE. Expression of VZV gE on the surface of cells did not interfere with VZV infection. HSV deleted for gE is impaired for cell-to-cell spread; VZV gE could not complement this activity in an HSV gE null mutant. VZV lacking the IDE binding domain of gE grew to peak titers nearly equivalent to parental virus; however, it was impaired for cell-to-cell spread and for infectivity with cell-free virus. VZV deleted for a region of gE that binds glycoprotein I could not replicate in cell culture unless grown in cells expressing gE. We conclude that the IDE binding domain is important for efficient cell-to-cell spread and infectivity of cell-free virus.

水痘带状疱疹病毒（VZV）糖蛋白E（gE）与糖蛋白I以及胰岛素降解酶（IDE）相互作用，胰岛素降解酶是该病毒的一种受体。我们发现，VZV gE缺失突变体只能在表达gE的细胞中生长。VZV gE在细胞表面的表达并不干扰VZV感染。缺失gE的单纯疱疹病毒（HSV）在细胞间传播方面存在缺陷；VZV gE不能在HSV gE缺失突变体中补充这一活性。缺乏gE的IDE结合域的VZV生长至峰值滴度几乎与亲本病毒相当；然而，它在细胞间传播以及对无细胞病毒的感染性方面存在缺陷。缺失gE中与糖蛋白I结合区域的VZV在细胞培养中无法复制，除非在表达gE的细胞中生长。我们得出结论，IDE结合域对于无细胞病毒的有效细胞间传播和感染性很重要。