Dijkstra J M, Visser N, Mettenleiter T C, Klupp B G
Institute of Molecular and Cellular Virology, Friedrich Loeffler Institutes, Federal Research Centre for Virus Diseases of Animals, Germany.
J Virol. 1996 Aug;70(8):5684-8. doi: 10.1128/JVI.70.8.5684-5688.1996.
Sequence analysis within BamHI fragment 3 of the pseudorabies virus (PrV) genome revealed an open reading frame homologous to the UL10 gene of herpes simplex virus. A rabbit antiserum directed against a synthetic oligopeptide representing the carboxy-terminal 18 amino acids of the predicted UL10 product recognized a major 45-kDa protein in lysates of purified Pr virions. In addition, a second protein of 90 kDa which could represent a dimeric form was observed. Enzymatic deglycosylation showed that the PrV UL10 protein is N glycosylated. Therefore, it was designated PrV gM according to its homolog in herpes simplex virus. A PrV mutant lacking ca. 60% of UL10 coding sequences was able to productively replicate on noncomplementing cells, demonstrating that PrV gM is not required for viral replication in cell culture. However, infectivity of the mutant virus was reduced and penetration was delayed, indicating a modulatory role of PrV gM in the initiation of infection.
伪狂犬病病毒(PrV)基因组BamHI片段3内的序列分析显示,存在一个与单纯疱疹病毒UL10基因同源的开放阅读框。一种针对代表预测的UL10产物羧基末端18个氨基酸的合成寡肽的兔抗血清,在纯化的Pr病毒粒子裂解物中识别出一种主要的45 kDa蛋白。此外,还观察到一种可能代表二聚体形式的90 kDa第二蛋白。酶促去糖基化表明,PrV UL10蛋白是N-糖基化的。因此,根据其在单纯疱疹病毒中的同源物,将其命名为PrV gM。一个缺失约60% UL10编码序列的PrV突变体能够在非互补细胞上高效复制,这表明PrV gM在细胞培养中的病毒复制过程中并非必需。然而,突变病毒的感染性降低,穿透延迟,表明PrV gM在感染起始过程中具有调节作用。