Eglin R P, Gugerli P, Wildy P
J Gen Virol. 1980 Jul;49(1):23-31. doi: 10.1099/0022-1317-49-1-23.
The delay in the replication of herpes simplex virus surviving u.v. irradiation occurs after the uncoating of virus, as judged by sensitivity to DNase. It occurs before translation, judged by the kinetics of appearance of various virus-specific proteins, and before transcription, judged by the detection of virus-specific RNA by in situ hybridization. Since the delays in both transcription and translation are reversed by photoreactivation, the simplest hypothesis is that pyrimidine dimers directly obstruct transcription;unless these are broken by photoreactivating enzymes, there will be transcriptional delay until reactivating processes have repaired the lesion. The u.v. sensitivities of the abilities to induce various enzymes (thymidine kinase, DNase and DNA polymerase) were only about four times less than that of infectivity. The The ability to induce the three enzymes was three times less sensitive than that of the structural antigen (Band II).
通过对脱氧核糖核酸酶（DNase）的敏感性判断，紫外线照射后存活的单纯疱疹病毒复制延迟发生在病毒脱壳之后。根据各种病毒特异性蛋白质出现的动力学判断，该延迟发生在翻译之前；根据原位杂交检测病毒特异性RNA判断，该延迟发生在转录之前。由于转录和翻译的延迟都可通过光复活作用逆转，最简单的假设是嘧啶二聚体直接阻碍转录；除非这些二聚体被光复活酶破坏，否则在修复损伤的再激活过程完成之前，转录将一直延迟。诱导各种酶（胸苷激酶、DNase和DNA聚合酶）的能力对紫外线的敏感性仅比感染性低约四倍。诱导这三种酶的能力比结构抗原（B带II）的敏感性低三倍。
