The UL20 gene product of pseudorabies virus functions in virus egress
The UL20 gene product of pseudorabies virus functions in virus egress
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DOI：
10.1128/jvi.71.7.5639-5646.1997
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发表时间：
1997-07-01
影响因子：
5.4
通讯作者：
Mettenleiter, TC
中科院分区：
文献类型：
--
作者：
Fuchs, W;Klupp, BG;Mettenleiter, TC
UL 20开放阅读框在不同的α疱疹病毒基因组中是位置保守的，并被预测编码整合膜蛋白。先前描述的单纯疱疹病毒1型（HSV-1）的UL 20（-）突变体表现出与病毒体在核周空间中的滞留相关的外出缺陷（J.D. Baines，P，L.沃德，G。Campadelli-Fiorio和B. Roizman，J. Virol，65：6414-6124，1991）。为了分析UL 20在一种相关但不同的疱疹病毒中的功能，我们通过插入突变构建了UL 20（-）伪狂犬病病毒（PrV）突变体。与HSV-1相似，发现UL 20（-）PrV在细胞间传播和从培养细胞释放方面均严重受损。这种缺陷的严重程度似乎是细胞类型依赖性的，在Vero细胞中比在人143 TK（-）细胞中更突出。令人惊讶的是，电子显微镜检查显示，在感染UL 20（-）PrV的Vero细胞的胞质囊泡中保留包膜病毒颗粒。这与UL 20（-）HSV-1突变体中的情况形成对比，UL 20（-）HSV-1突变体在Vero细胞的核周池中积累病毒粒子。因此，PrV和HSV-1的UL 20基因产物似乎参与病毒外出的不同步骤，在不同的细胞内区室中起作用，这可能是由UL 20蛋白本身的不同功能或由其他病毒基因产物介导的PrV和HSV-1的通常不同的外出途径引起的。
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, 65:6414-6124, 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.