Rauh I, Mettenleiter T C
Federal Research Centre for Virus Diseases of Animals, Tübingen, Germany.
J Virol. 1991 Oct;65(10):5348-56. doi: 10.1128/JVI.65.10.5348-5356.1991.
Pseudorabies virus (PrV) glycoproteins gII and gp50 are major constituents of the viral envelope and targets of neutralizing monoclonal antibodies. Both are homologs of essential glycoproteins found in herpes simplex virus, gB (gII) and gD (gp50). We recently isolated a gII-negative PrV deletion mutant on complementing cell lines and established the essential character of gII for PrV replication (I. Rauh, F. Weiland, F. Fehler, G. Keil, and T.C. Mettenleiter, J. Virol. 65: 621-631, 1991). In this report, we describe the isolation of a gp50-negative PrV mutant after constructing cell lines that constitutively express gp50 and phenotypically complement the gp50 defect. Analysis of the gp50- mutant proved that gp50 is essential for PrV replication. Further studies showed that both gII and gp50 are required for viral penetration into target cells. The penetration defect in the gII and gp50 deletion mutants could be overcome by experimental polyethylene glycol-induced membrane fusion. Surprisingly, whereas gII proved to be essential for both penetration and cell-cell spread of the virus, gp50 was required only for penetration and appeared dispensable for direct cell-cell spread.
伪狂犬病病毒（PrV）糖蛋白gII和gp50是病毒包膜的主要成分以及中和性单克隆抗体的靶标。二者均为单纯疱疹病毒中必需糖蛋白gB（gII）和gD（gp50）的同源物。我们最近在互补细胞系上分离出了一株gII阴性的PrV缺失突变体，并确定了gII对PrV复制的必需特性（I. 劳赫、F. 魏兰德、F. 费勒、G. 凯尔和T.C. 梅滕莱特，《病毒学杂志》65: 621 - 631, 1991）。在本报告中，我们描述了在构建组成型表达gp50并在表型上互补gp50缺陷的细胞系后，分离出一株gp50阴性的PrV突变体。对gp50突变体的分析证明gp50对PrV复制至关重要。进一步研究表明，gII和gp50都是病毒侵入靶细胞所必需的。gII和gp50缺失突变体中的侵入缺陷可通过实验性聚乙二醇诱导的膜融合来克服。令人惊讶的是，虽然gII被证明对病毒的侵入和细胞间传播都至关重要，但gp50仅对侵入是必需的，而对于直接的细胞间传播似乎是可有可无的。
