Tucker A G, Docherty J J
Infect Immun. 1975 Mar;11(3):556-62. doi: 10.1128/iai.11.3.556-562.1975.
A cell line that normally supports the replication of herpes simplex virus types 1 and 2 became resistant to these viruses after transformation by simian adenovirus 7. Kinetic studies of the mechanism of resistance demonstrated that both herpesviruses were able to attach to the transformed cells and express some early genomic functions, as demonstrated by the presence of low levels of viral thymidine kinase. However, isopycnic centrifugation studies of the abortive system failed to detect viral deoxyribonucleic acid synthesis, whereas indirect immunofluorescent studies of viral proteins revealed that less than 10 per cent of the cells contained these viral macromolecules at any given time. Collectively the data suggest that after transformation by simian adenovirus 7 these cells are altered so as to render them resistant or incapable of supporting the growth of herpes simplex virus types 1 and 2. The results further suggest that the block occurs after viral absorption and prior to viral deoxyribonucleic acid synthesis.
一种通常支持1型和2型单纯疱疹病毒复制的细胞系,在被猴腺病毒7转化后,对这些病毒产生了抗性。对这种抗性机制的动力学研究表明,两种疱疹病毒都能够附着在转化细胞上并表达一些早期基因组功能,这可通过低水平的病毒胸苷激酶的存在得以证明。然而,对这种流产系统的等密度离心研究未能检测到病毒脱氧核糖核酸的合成,而对病毒蛋白的间接免疫荧光研究表明,在任何给定时间,不到10%的细胞含有这些病毒大分子。总体而言,数据表明,在被猴腺病毒7转化后,这些细胞发生了改变,从而使其对1型和2型单纯疱疹病毒具有抗性或无法支持其生长。结果还表明,这种阻断发生在病毒吸附之后、病毒脱氧核糖核酸合成之前。