Sanjuan N, Porrás A, Otero J, Perazzo S
Laboratory of Experimental Pathology, Department of Microbiology, University of Buenos Aires School of Medicine, Buenos Aires, Argentina.
J Virol. 2001 Mar;75(6):2891-9. doi: 10.1128/JVI.75.6.2891-2899.2001.
Thymomas induced by polyomavirus strain PTA in mice are known to express the major capsid protein VP-1. Since the expression of a late structural protein such as VP-1 is considered a sign of virus replication, the present work attempted to clarify the implication of the presence of this protein in tumor cells. Electron microscopy of tumors showed a striking absence of viral particles in the vast majority of the cells. However, immunoelectron microscopy of the same samples demonstrated intranuclear VP-1 in most cells despite the absence of viral particles. Very little infectious virus was recovered from tumors. A change in the electrophoretic mobility of VP-1 from thymomas was detected compared with VP-1 from productively infected cells. The data presented in this work prove that the expression of VP-1 in polyomavirus-induced tumors is not synonymous with the presence of infectious virus, suggesting a possible defect in viral encapsidation.
已知多瘤病毒株PTA在小鼠中诱导产生的胸腺瘤会表达主要衣壳蛋白VP - 1。由于像VP - 1这样的晚期结构蛋白的表达被认为是病毒复制的标志,因此本研究试图阐明该蛋白在肿瘤细胞中的存在所蕴含的意义。对肿瘤进行电子显微镜检查发现,绝大多数细胞中明显没有病毒颗粒。然而,对相同样本进行免疫电子显微镜检查显示,尽管没有病毒颗粒,但大多数细胞的细胞核内存在VP - 1。从肿瘤中回收的感染性病毒极少。与来自有效感染细胞的VP - 1相比,检测到胸腺瘤中VP - 1的电泳迁移率发生了变化。本研究呈现的数据证明,多瘤病毒诱导的肿瘤中VP - 1的表达并不等同于感染性病毒的存在,这表明病毒衣壳化可能存在缺陷。