Rommelaere J, Ward D C
Nucleic Acids Res. 1982 Apr 24;10(8):2577-96. doi: 10.1093/nar/10.8.2577.
The effect of UV-irradiation on the conversion of the single-stranded DNA of the parvovirus Minute-Virus-of-Mice (MVM) to duplex Replicative Forms (RF) was studied after infection of mouse A9 fibroblasts. UV-irradiation of the virus prior to infection of unirradiated cells resulted in a dose-dependent, single-hit, inhibition of RF formation. Restriction fragment analysis indicated that this inhibition could be ascribed to the introduction of absolute blocks which prevent elongation of the newly synthesized complementary strand. Cell exposure to UV-light prior to infection with UV-irradiated MVM enhanced the fraction of input viral DNA which was converted to RF. This enhancement required de novo protein synthesis during the interval between cell irradiation and virus infection. These results suggest that DNA replication constitutes a target in the viral life cycle that leads to the UV-enhanced Reactivation of virus survival, however, they do not permit us to identify the step of RF formation which is enhanced in UV-pretreated cells.
在感染小鼠A9成纤维细胞后，研究了紫外线照射对细小病毒小鼠微小病毒（MVM）单链DNA转化为双链复制形式（RF）的影响。在感染未照射细胞之前对病毒进行紫外线照射，导致RF形成受到剂量依赖性、单次打击的抑制。限制性片段分析表明，这种抑制可归因于引入了绝对阻断，从而阻止了新合成互补链的延伸。在用紫外线照射的MVM感染之前，细胞暴露于紫外线下可提高转化为RF的输入病毒DNA的比例。这种增强需要在细胞照射和病毒感染之间的间隔期进行从头蛋白质合成。这些结果表明，DNA复制构成了病毒生命周期中的一个靶点，导致紫外线增强病毒存活的复活，然而，它们不允许我们确定在紫外线预处理细胞中增强的RF形成步骤。
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