Fuchs W, Klupp B G, Granzow H, Mettenleiter T C
Institutes of Molecular and Cellular Virology, Friedrich-Loeffler-Institutes, Federal Research Centre for Virus Diseases of Animals, Insel Riems, Germany.
J Virol. 1997 Jul;71(7):5639-46. doi: 10.1128/JVI.71.7.5639-5646.1997.
The UL20 open reading frame is positionally conserved in different alphaherpesvirus genomes and is predicted to encode an integral membrane protein. A previously described UL20- mutant of herpes simplex virus type 1 (HSV-1) exhibited a defect in egress correlating with retention of virions in the perinuclear space (J. D. Baines, P. L. Ward, G. Campadelli-Fiume, and B. Roizman, J. Virol. 65:6414-6424, 1991). To analyze UL20 function in a related but different herpesvirus, we constructed a UL20- pseudorabies virus (PrV) mutant by insertional mutagenesis. Similar to HSV-1, UL20- PrV was found to be severely impaired in both cell-to-cell spread and release from cultured cells. The severity of this defect appeared to be cell type dependent, being more prominent in Vero than in human 143TK- cells. Surprisingly, electron microscopy revealed the retention of enveloped virus particles in cytoplasmic vesicles of Vero cells infected with UL20- PrV. This contrasts with the situation in the UL20- HSV-1 mutant, which accumulated virions in the perinuclear cisterna of Vero cells. Therefore, the UL20 gene products of PrV and HSV-1 appear to be involved in distinct steps of viral egress, acting in different intracellular compartments. This might be caused either by different functions of the UL20 proteins themselves or by generally different egress pathways of PrV and HSV-1 mediated by other viral gene products.
UL20开放阅读框在不同的α疱疹病毒基因组中位置保守，预计编码一种整合膜蛋白。先前描述的1型单纯疱疹病毒（HSV-1）的UL20突变体在出芽过程中表现出缺陷，这与病毒粒子在核周空间的滞留相关（J. D. 贝恩斯、P. L. 沃德、G. 坎帕代利-菲乌梅和B. 罗伊兹曼，《病毒学杂志》65:6414 - 6424，1991）。为了分析UL20在一种相关但不同的疱疹病毒中的功能，我们通过插入诱变构建了一个UL20缺失的伪狂犬病病毒（PrV）突变体。与HSV-1类似，发现UL20缺失的PrV在细胞间传播和从培养细胞中释放方面均严重受损。这种缺陷的严重程度似乎取决于细胞类型，在Vero细胞中比在人143TK -细胞中更明显。令人惊讶的是，电子显微镜显示在感染UL20缺失的PrV的Vero细胞的细胞质囊泡中存在包膜病毒粒子的滞留。这与UL20缺失的HSV-1突变体的情况形成对比，后者在Vero细胞的核周池中积累病毒粒子。因此，PrV和HSV-1的UL20基因产物似乎参与病毒出芽的不同步骤，在不同的细胞内区室中发挥作用。这可能是由UL20蛋白本身的不同功能引起的，也可能是由PrV和HSV-1由其他病毒基因产物介导的一般不同的出芽途径引起的。
