Meindl A, Osterrieder N
Institute of Molecular and Cellular Virology, Friedrich-Loeffler-Institutes, Federal Research Center for Virus Diseases of Animals, D-17498 Insel Riems, Germany.
J Virol. 1999 Apr;73(4):3430-7. doi: 10.1128/JVI.73.4.3430-3437.1999.
Experiments were conducted to analyze the equine herpesvirus 1 (EHV-1) gene 68 product which is encoded by the EHV-1 Us2 homolog. An antiserum directed against the amino-terminal 206 amino acids of the EHV-1 Us2 protein specifically detected a protein with an Mr of 34,000 in cells infected with EHV-1 strain RacL11. EHV-1 strain Ab4 encodes a 44,000-Mr Us2 protein, whereas vaccine strain RacH, a high-passage derivative of RacL11, encodes a 31,000-Mr Us2 polypeptide. Irrespective of its size, the Us2 protein was incorporated into virions. The EHV-1 Us2 protein localized to membrane and nuclear fractions of RacL11-infected cells and to the envelope fraction of purified virions. To monitor intracellular trafficking of the protein, the green fluorescent protein (GFP) was fused to the carboxy terminus of the EHV-1 Us2 protein or to a truncated Us2 protein lacking a stretch of 16 hydrophobic amino acids at the extreme amino terminus. Both fusion proteins were detected at the plasma membrane and accumulated in the vicinity of nuclei of transfected cells. However, trafficking of either GFP fusion protein through the secretory pathway could not be demonstrated, and the EHV-1 Us2 protein lacked detectable N- and O-linked carbohydrates. Consistent with the presence of the Us2 protein in the viral envelope and plasma membrane of infected cells, a Us2-negative RacL11 mutant (L11DeltaUs2) exhibited delayed penetration kinetics and produced smaller plaques compared with either wild-type RacL11 or a Us2-repaired virus. After infection of BALB/c mice with L11DeltaUs2, reduced pathogenicity compared with the parental RacL11 virus and the repaired virus was observed. It is concluded that the EHV-1 Us2 protein modulates virus entry and cell-to-cell spread and appears to support sustained EHV-1 replication in vivo.
开展了实验以分析由马疱疹病毒1型(EHV-1)Us2同源物编码的EHV-1基因68产物。一种针对EHV-1 Us2蛋白氨基末端206个氨基酸的抗血清在感染EHV-1毒株RacL11的细胞中特异性检测到一种Mr为34,000的蛋白。EHV-1毒株Ab4编码一种44,000-Mr的Us2蛋白,而疫苗毒株RacH(RacL11的高传代衍生物)编码一种31,000-Mr的Us2多肽。无论其大小如何,Us2蛋白都被整合到病毒粒子中。EHV-1 Us2蛋白定位于RacL11感染细胞的膜和核部分以及纯化病毒粒子的包膜部分。为了监测该蛋白在细胞内的运输,绿色荧光蛋白(GFP)与EHV-1 Us2蛋白的羧基末端或与在最氨基末端缺少一段16个疏水氨基酸的截短Us2蛋白融合。两种融合蛋白都在质膜上被检测到,并在转染细胞的细胞核附近积累。然而,未证明任何一种GFP融合蛋白通过分泌途径运输,并且EHV-1 Us2蛋白缺乏可检测到的N-和O-连接碳水化合物。与Us2蛋白存在于感染细胞的病毒包膜和质膜中一致,与野生型RacL11或Us2修复病毒相比,Us2阴性的RacL11突变体(L11DeltaUs2)表现出延迟的穿透动力学并且产生较小的噬斑。用L11DeltaUs2感染BALB/c小鼠后,观察到与亲本RacL11病毒和修复病毒相比致病性降低。结论是EHV-1 Us2蛋白调节病毒进入和细胞间传播,并且似乎支持EHV-1在体内的持续复制。