Repair of Psoralen-treated DNA by Genetic Recombination in Human Cells Infected with Herpes Simplex Virus

摘要: Herpes simplex virus type 1 was treated with 4,5'-8-trimethylpsoralen (psoralen) plus near-ultraviolet light in order to produce lesions (monoadducts and DNA cross-links) the viral DNA. Human fibroblasts were infected by damaged under conditions which either a single particle or several particles entered given cell, fraction of virus-producing cells determined. This significantly greater for multiply than singly cells, indicating that psoralen are repaired more efficiently present homologous, (multiplicity reactivation). Evidence is presented herpes may code functions participate its own repair, both during multiplicity reactivation repair occurs cells: (a) host deficient induced (xeroderma pigmentosum) cross-linking agent mitomycin C (Fanconi's anemia) exhibited normal levels psoralen-treated virus; (b) while xeroderma pigmentosum have been previously shown be adenovirus infection, at near these same cells. Recombination between genetically marked pairs viruses found increase after treatment parental psoralen, suggesting damage stimulates genetic recombination. stimulation provides convincing evidence pathway recombination genomes can lead production viable virus.