Enhanced Survival of Ultraviolet-Damaged Parvovirus LuIII and Herpes Virus in Carcinogen Pretreated Transformed Human Cells
An increased survival of UV (254 nm-damaged DNA viruses (Herpes, Adenovirus and SV40) occurs in mammalian cells treated prior to infection by low doses of physical (UV and X-rays) or chemical carcinogens1–6. This increase is more pronounced when the treatment is given a few days before infection. The rate of forward mutations (Herpes virus)7 and of backward mutations (SV40)8 is significantly higher in the reactivated than in the control viruses, indicating that the underlying process could be, as in bacteria a manifestation of an error-prone mode of DNA repair9–10. In order to study such an inducible repair process in mammalian cells without any interference with excision repair mechanisms, we analysed the reactivation of an UV-damaged single-stranded DNA virus (parvovirus LuIII) in human cells treated by different carcinogens. For comparison the reactivation of UV-damaged Herpes virus (HSV) was examined in parallel cultures.
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