Mallory S, Sommer M, Arvin A M
Department of Pediatrics and Microbiology/Immunology, Stanford University School of Medicine, CA 94305, USA.
J Infect Dis. 1998 Nov;178 Suppl 1:S22-6. doi: 10.1086/514277.
The contributions of the glycoproteins gI (ORF67) and gE (ORF68) to varicella-zoster virus (VZV) replication were investigated in deletion mutants made by using cosmids with VZV DNA derived from the Oka strain. These experiments demonstrated that gI was not required for VZV replication in vitro but gE appeared to be. Although VZV gI was not required, its deletion or mutation resulted in a significant decrease in infectious virus yields, and it disrupted syncytial formation and altered the conformation and distribution of gE in infected cells. Normal cell-to-cell spread and replication kinetics were restored when gI was expressed from a non-native locus in the VZV genome. The expression of intact gI, the ORF67 gene product, is required for efficient VZV replication.
利用含有源自Oka株水痘-带状疱疹病毒(VZV)DNA的黏粒构建的缺失突变体,研究了糖蛋白gI(开放阅读框67)和gE(开放阅读框68)对VZV复制的作用。这些实验表明,体外VZV复制不需要gI,但gE似乎是必需的。虽然不需要VZV gI,但其缺失或突变导致感染性病毒产量显著降低,破坏了多核巨细胞形成,并改变了gE在感染细胞中的构象和分布。当gI从VZV基因组中的非天然位点表达时,正常的细胞间传播和复制动力学得以恢复。完整的gI(开放阅读框67基因产物)的表达是高效VZV复制所必需的。