Abstract
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 bacteria3,4. 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 mechanism2,6. Previous investigations have raised the possibility of a host cell reactivation system in mammalian cells7–13. 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.
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AARONSON, S., LYTLE, C. Decreased Host Cell Reactivation of Irradiated SV40 Virus in Xeroderma Pigmentosum. Nature 228, 359–361 (1970). https://doi.org/10.1038/228359a0
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DOI: https://doi.org/10.1038/228359a0
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