Witt D J
Arch Virol. 1984;79(1-2):95-107. doi: 10.1007/BF01314307.
The nuclear polyhedrosis virus (Baculovirus) of Galleria mellonella (Pryalidae: Lepidoptera) was used to investigate the capability of cultured insect cells to repair ultraviolet (UV) induced damage in the viral genome. When assayed by the formation of plaques in the cell line TN-368, the survival of the virus was found to decrease linearly with increased ultraviolet exposure. The infectious capacity of UV-irradiated virions was significantly restored after exposing the TN-368 monolayers to either photoreactivation conditions (white fluorescent and black light) or to UV-enhanced reactivation conditions (far ultraviolet radiation). Using both types of repair sequentially resulted in higher reactivation than when either was used alone. These results indicate that pyrimidine dimers are the major factor responsible for inactivation of this virus by UV radiation but that other photolesions not repairable by photoreactivation partially account for the inactivation of the virus.
利用大蜡螟（螟蛾科：鳞翅目）的核型多角体病毒（杆状病毒）来研究培养的昆虫细胞修复紫外线（UV）诱导的病毒基因组损伤的能力。通过在TN - 368细胞系中形成噬菌斑进行检测时，发现病毒的存活率随紫外线照射剂量的增加呈线性下降。在将TN - 368单层细胞暴露于光复活条件（白色荧光和黑光）或紫外线增强复活条件（远紫外线辐射）后，紫外线照射的病毒粒子的感染能力得到显著恢复。依次使用这两种修复方式比单独使用任何一种方式能产生更高的复活率。这些结果表明嘧啶二聚体是该病毒被紫外线辐射灭活的主要因素，但其他无法通过光复活修复的光损伤部分导致了病毒的灭活。
