The study of DNA-repair defects using [125I]iododeoxycytidine incorporation as an assay for the growth of herpes simplex virus.
[125I]Iododeoxycytidine incorporation was used to measure herpes virus (HSV-1) DNA synthesis following specific DNA damage. Xeroderma pigmentosum fibroblasts were less able to replicate UV-irradiated viral DNA than were normal fibroblasts, indicating the necessity for excision repair for the survival of UV-irradiated virus. Because of its rapidity and ease of quantitation, this assay had advantages over standard viral mediated assays of DNA excision repair. It was possible to monitor viral replication as a function of the cellular cell cycle. Other genetic defects which have been proposed to reflect deficiencies in DNA-repair capacity were not detected by this assay. DNA-repair inhibitors, caffeine and 3-aminobenzamide, also did not show synergistic lethal effects on the replication of damaged viral DNA.
D001260:Ataxia Telangiectasia / Q000235:genetics; D001816:Bloom Syndrome / Q000235:genetics; D001972:Bromodeoxycytidine / Q000031:analogs & derivatives; D002110:Caffeine / Q000494:pharmacology; D002453:Cell Cycle; D002478:Cells, Cultured; D004260:DNA Repair; D003841:Deoxycytidine / Q000031:analogs & derivatives*; D006801:Humans; D006816:Huntington Disease / Q000235:genetics; D018139:Simplexvirus / Q000254:growth & development*; D014466:Ultraviolet Rays; D014779:Virus Replication / Q000187:drug effects / Q000528:radiation effects
D003841:Deoxycytidine; D001972:Bromodeoxycytidine; C011288:ibacitabine; D002110:Caffeine