Vos J M, Rommelaere J
Biochimie. 1982 Aug-Sep;64(8-9):839-44. doi: 10.1016/s0300-9084(82)80139-9.
The replication of the single-stranded DNA of parvovirus Minute-Virus-of-MIce (MVM) was depressed when virus was exposed to UV-light prior to infection of mouse fibroblasts. Most of the viral DNA containing pyrimidine dimers was permanently blocked in its conversion to double-stranded replicative forms (RF). Yet dimers might be tolerated to a low extent, considering that a minor fraction of parental RF molecules was sensitive to the action of the UV-specific endonuclease V of bacteriophage T4, UV-irradiation of the cells prior to infection with UV-damaged MVM increased the levels of both parental RF and total viral DNA synthesized. The sensitivity of parental RF molecules to the UV-specific endonuclease was little enhanced by preirradiation of the cells and did not appear to be sufficient to account for the stimulation of RF formation in those cultures. Since parvoviral single-stranded DNA is not a substrate for nucleotidyl excision repair, one interpretation of these results would be that the process(es) activated in preirradiated cells overcome(s) barriers to viral DNA replication other than elongation blocks at pyrimidine dimers. Alternatively, pyrimidine dimers tolerated in pretreated cultures might become protected from attack by the UV-endonuclease.
在小鼠成纤维细胞感染前，将微小病毒属小鼠微小病毒（MVM）的单链DNA暴露于紫外线下，其复制受到抑制。大多数含有嘧啶二聚体的病毒DNA在转化为双链复制形式（RF）时被永久阻断。然而，考虑到一小部分亲本RF分子对噬菌体T4的紫外线特异性内切酶V的作用敏感，二聚体可能在一定程度上是可以耐受的，在用紫外线损伤的MVM感染前对细胞进行紫外线照射，会增加亲本RF和合成的总病毒DNA的水平。细胞预照射对亲本RF分子对紫外线特异性内切酶的敏感性增强作用很小，似乎不足以解释这些培养物中RF形成的刺激现象。由于细小病毒单链DNA不是核苷酸切除修复的底物，这些结果的一种解释是，预照射细胞中激活的过程克服了病毒DNA复制的障碍，而不是嘧啶二聚体处的延伸阻滞。或者，预处理培养物中耐受的嘧啶二聚体可能受到保护，免受紫外线内切酶的攻击。
