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.
Intine
R V
RV
Department of Biology, McMaster University, Hamilton, Ontario, Canada.
Rainbow
A J
AJ
D004260:DNA Repair / Q000502:physiology*; D004279:DNA, Viral / Q000528:radiation effects*; D006801:Humans; D009154:Mutation; D018139:Simplexvirus / Q000201:enzymology* / Q000235:genetics / Q000528:radiation effects; D013937:Thymidine Kinase / Q000235:genetics / Q000378:metabolism*; D014466:Ultraviolet Rays; D010948:Viral Plaque Assay; D014983:Xeroderma Pigmentosum
D004279:DNA, Viral; D013937:Thymidine Kinase