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Evidence for an involvement of thymidine kinase in the excision repair of ultraviolet‐irradiated herpes simplex virus in human cells

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.