Coppey J, Nocentini S
J Gen Virol. 1976 Jul;32(1):1-15. doi: 10.1099/0022-1317-32-1-1.
The rate of virus DNA synthesis and the production of infectious virus are impaired in stationary monkey kidney CV-I cells irradiated with u.v. before infection with herpes simplex virus (HSV). The inhibition of HSV multiplication is due to u.v.-induced damage in cell DNA. CV-I cells recover their capacity to support HSV growth during the 40 to 48 h after irradiation, and the final virus yield is enhanced by a factor of 10. The time course of the recovery is similar to that of the excision repair process occurring in u.v.-irradiated mammalian cells. Caffeine, hydroxyurea and cycloheximide inhibit the recovery. Fluorodeoxyuridine is without effect. A small but significant amount of labelled dThd coming from irradiated cell DNA is incorporated into virus DNA. HSV specified thymidine kinase seems to be more effective for virus DNA synthesis in irradiated than in control cells.
在用单纯疱疹病毒(HSV)感染之前,对处于静止期的猴肾CV - I细胞进行紫外线照射后,病毒DNA合成速率和感染性病毒的产生均受到损害。HSV增殖的抑制是由于紫外线诱导的细胞DNA损伤所致。CV - I细胞在照射后40至48小时内恢复其支持HSV生长的能力,最终病毒产量提高了10倍。恢复的时间进程与紫外线照射的哺乳动物细胞中发生的切除修复过程相似。咖啡因、羟基脲和环己酰亚胺会抑制恢复。氟脱氧尿苷则没有效果。少量但显著的来自照射细胞DNA的标记dThd被掺入病毒DNA中。HSV特异性胸苷激酶在受照射细胞中对病毒DNA合成似乎比在对照细胞中更有效。