Bubley G J, Crumpacker C S, Schnipper L E
Cancer Res. 1984 May;44(5):1813-8.
The nucleoside analogue 1-beta-D-arabinofuranosylcytosine (ara-C) is incorporated into herpes simplex virus type 1 (HSV-1) DNA, and this correlates with inhibition of virus replication. The technique of Weigle-type reactivation (WR) was used to compare the ability of induced cellular DNA repair pathways to recognize or repair ara-C incorporated into HSV-1 DNA and ultraviolet (UV)-irradiated virus DNA (254 nm). Pretreatment of monkey cells with low-fluence UV irradiation, growth in cis-dichlorodiammineplatinum(II), or growth in ara-C followed by infection after a 24-hr incubation period resulted in enhanced survival of UV-irradiated HSV-1. Under the same experimental conditions, no reactivation of HSV-1 inactivated by growth in ara-C is observed. Comparisons between uninfected Vero cells exposed to UV irradiation (30 J/m2) or grown in 10(-6) M ara-C demonstrated repair replication in irradiated cells, whereas there was no evidence for DNA repair at various time intervals following removal of the nucleoside analogue. These observations suggest that, once ara-C is incorporated into HSV-1 or eukaryotic DNA, it is not recognized as a repairable lesion within the limits of the DNA repair assays used in these studies.
核苷类似物1-β-D-阿拉伯呋喃糖基胞嘧啶（ara-C）可掺入单纯疱疹病毒1型（HSV-1）的DNA中，这与病毒复制的抑制相关。采用韦格尔型复活（WR）技术，比较诱导的细胞DNA修复途径识别或修复掺入HSV-1 DNA以及紫外线（UV）照射（254 nm）的病毒DNA中的ara-C的能力。用低通量紫外线照射预处理猴细胞、在顺二氯二氨铂（II）中生长或在ara-C中生长，然后在24小时孵育期后进行感染，可提高紫外线照射的HSV-1的存活率。在相同实验条件下，未观察到因在ara-C中生长而失活的HSV-1的复活。对暴露于紫外线照射（30 J/m2）或在10(-6) M ara-C中生长的未感染Vero细胞进行比较，结果表明受照射细胞存在修复复制，而在去除核苷类似物后的不同时间间隔内均未发现DNA修复的证据。这些观察结果表明，一旦ara-C掺入HSV-1或真核生物的DNA中，在这些研究中所使用的DNA修复检测范围内，它不会被识别为可修复的损伤。
