Decreased host cell reactivation of irradiated SV40 Virus in Xeroderma pigmentosum

BACTERIA possess enzyme systems for repairing in the dark the damage caused by ultraviolet irradiation¹ in which damaged regions of DNA are excised and replaced³. Damage to an infecting phage can also be repaired. This capacity, known as host cell reactivation (HCR), is manifested by the lowered survival of ultraviolet irradiated phages in radiation-sensitive mutant host bacteria^3,4. Mammalian cells also possess repair systems. In xeroderma pigmentosum, a genetic disease associated with unusually high sensitivity to sunlight and a greatly increased susceptibility to carcinomas and melanomas of the skin, the capacity of fibroblast cells for repair is much lower than that of normal fibroblasts⁵. Recent evidence suggests that xeroderma pigmentosum cells are defective in the first reaction of the DNA repair mechanism^2,6. Previous investigations have raised the possibility of a host cell reactivation system in mammalian cells ^7-13. We have shown directly that normal human cells have HCR capacity by comparing the ultraviolet sensitivities of two viral functions of the DNA tumour virus SV40 - transformation and T-antigen induction - in normal and xeroderma pigmentosum cells.