Intine R V, Rainbow A J
Department of Biology, McMaster University, Hamilton, Ontario, Canada.
Environ Mol Mutagen. 1990;15(1):19-23. doi: 10.1002/em.2850150104.
A wild-type strain of herpes simplex virus type 1 (HSV-1:KOS) encoding a functional thymidine kinase (tk+) and a tk- mutant strain (HSV-1:PTK3B) were used to study the role of the viral tk in the repair of UV-irradiated HSV-1 in human cells. UV survival of HSV-1:PTK3B was substantially reduced compared with that of HSV-1:KOS when infecting normal human cells. In contrast, the UV survival of HSV-1:PTK3B was similar to that of HSV-1:KOS when infecting excision repair-deficient cells from a xeroderma pigmentosum patient from complementation group A. These results suggest that the repair of UV-irradiated HSV-1 in human cells depends, in part at least, on expression of the viral tk and that the repair process influenced by tk activity is excision repair or a process dependent on excision repair.
一株编码功能性胸苷激酶（tk+）的野生型单纯疱疹病毒1型（HSV-1:KOS）和一株tk-突变株（HSV-1:PTK3B）被用于研究病毒tk在人细胞中紫外线照射的HSV-1修复中的作用。当感染正常人细胞时，与HSV-1:KOS相比，HSV-1:PTK3B的紫外线存活率显著降低。相反，当感染来自A互补组的着色性干皮病患者的切除修复缺陷细胞时，HSV-1:PTK3B的紫外线存活率与HSV-1:KOS相似。这些结果表明，人细胞中紫外线照射的HSV-1的修复至少部分取决于病毒tk的表达，并且受tk活性影响的修复过程是切除修复或依赖于切除修复的过程。
