Lytle C D, Day R S, Hellman K B, Bockstahler L E
Mutat Res. 1976 Sep;36(3):257-64. doi: 10.1016/0027-5107(76)90235-9.
The capacity of monolayers of both normal human and xeroderma pigmentosum (XP) filbroblasts to support plaque formation by herpes simplex virus was decreased when the monolayers were ultraviolet (UV) irradiated and infected with virus. Fibroblasts of XP complementation groups A, B, and D were sensitive to UV, being 4-6 fold more sensitive than either fibroblasts of XP complementation group C or fibroblasts from a normal individual. When the monolayers were irradiated 4 days prior to infection, the capacity of normal fibroblasts to support herpes virus growth recovered, whereas the capacity of the XP strains decreased further compared to that measured when infection immediately followed irradiation. Concurrent experiments with UV-irradiated herpes virus showed that the survival of this virus did not increase when infection by irradiated virus immediately followed irradiation of the monolayers. However, if the monolayers were irradiated 4 days prior to infection, the survival of this virus increased by a factor of nearly 2. Such Weigle reactivation (WR) occurred at lower fluences to the XP fibroblasts than to normal fibroblasts, suggesting that WR results from residual cellular DNA damage left after excision repair.
当正常人成纤维细胞和着色性干皮病(XP)成纤维细胞单层经紫外线(UV)照射并感染病毒时,它们支持单纯疱疹病毒形成蚀斑的能力会降低。XP互补组A、B和D的成纤维细胞对紫外线敏感,比XP互补组C的成纤维细胞或正常个体的成纤维细胞敏感4至6倍。当单层细胞在感染前4天进行照射时,正常成纤维细胞支持疱疹病毒生长的能力得以恢复,而与感染紧跟在照射后所测得的能力相比,XP菌株的能力则进一步下降。对紫外线照射的疱疹病毒进行的同步实验表明,当单层细胞照射后立即用照射过的病毒进行感染时,这种病毒的存活率并未增加。然而,如果单层细胞在感染前4天进行照射,这种病毒的存活率会增加近2倍。这种韦格勒复活(WR)现象在XP成纤维细胞上发生时所需的通量低于正常成纤维细胞,这表明WR是由切除修复后残留的细胞DNA损伤导致的。