Enhanced survival of ultraviolet-irradiated herpes simplex virus in carcinogen-pretreated cells

Abstract

WHEN CV-1 monkey kidney host cells are exposed to low doses of ultraviolet (UV) or X-ray radiation, or to photodynamic treatment before infection with herpes simplex virus type 1 (HSV), the survival of UV-irradiated virus is increased^1–3. This increase is more pronounced if the time interval between cell UV-irradiation and virus infection is increased by a few days⁴. A similarly increased survival of UV-damaged phage λ is observed in bacteria damaged by UV, X rays, thymine starvation, exposure to mitomycin C, or thermal shift of tif-1 mutants⁵. Moreover, it has been shown that enhanced survival of UV-damaged phage λ occurred in bacteria previously treated with enzymatically activated aflatoxin B₁, a potent hepatocarcinogen⁶. The purpose of this study was to determine whether treatment of CV-1 cells with carcinogens would result in enhanced survival of UV-inactivated HSV. We chose for this purpose (1) aflatoxin B₁ because, after treatment with this activated mycotoxin, human fibroblast cells exhibit a UV-like repair replication, the extent of which is at the very most 20% of that observed after UV irradiation⁷, and (2) acetylamino-fluorene (AAF) and its derivatives, n-acetoxy-2-AAF and n-hydroxy-2-AAF, as these derivatives are known to be active intermediates in the carcinogenic activity of the parental compound⁸, and because, in n-acetoxy-AAF-treated human cells, there is a UV-like repair response⁹. Virus reactivation was assayed in the same manner as that used in previous investigations of radiation-enhanced reactivation^1–4.