Nishiyama Y, Rapp F
J Gen Virol. 1981 Jan;52(Pt 1):113-9. doi: 10.1099/0022-1317-52-1-113.
Human embryonic fibroblasts infected with u.v.-irradiated herpes simplex virus type 2 (HSV-2, strain 186) and maintained at 40.5 degrees C did not yield detectable virus. Virus synthesis was induced by temperature shift-down to 36.5 degrees C. The induced virus grew very poorly and was inactivated very rapidly at 40.5 degrees C. Non-irradiated virus failed to establish latency at 40.5 degrees C in infected cells. Enhanced reactivation of HSV-2 was observed when latently infected cultures were superinfected with human cytomegalovirus (HCMV) or irradiated with a small dose of u.v. light at the time of temperature shift-down. HCMV did not enhance synthesis of HSV-2 during a normal growth cycle but did enhance synthesis of u.v.-irradiated HSV-2. These observations suggest that in this in vitro latency system, some HSV genomes damaged by u.v. irradiation were maintained in a non-replicating state without being destroyed or significantly repaired.
感染紫外线照射的2型单纯疱疹病毒（HSV-2，186株）并维持在40.5摄氏度的人胚胎成纤维细胞未产生可检测到的病毒。通过温度下调至36.5摄氏度诱导病毒合成。诱导产生的病毒生长非常缓慢，并且在40.5摄氏度时迅速失活。未照射的病毒在感染细胞中于40.5摄氏度时未能建立潜伏状态。当潜伏感染的培养物在温度下调时被人巨细胞病毒（HCMV）超感染或用小剂量紫外线照射时，观察到HSV-2的再激活增强。HCMV在正常生长周期中不增强HSV-2的合成，但确实增强紫外线照射的HSV-2的合成。这些观察结果表明，在这个体外潜伏系统中，一些被紫外线照射损伤的HSV基因组以非复制状态维持，而没有被破坏或显著修复。
