HOST-CELL REACTIVATION STUDIES WITH EPIDERMAL-CELLS OF MICE SENSITIVE AND RESISTANT TO CARCINOGENESIS

  • 1 January 1984
    • journal article
    • research article
    • Vol. 44  (3) , 893-895
Abstract
Primary epidermal cells from AKR, BALB/c, CD-1 and SENCAR mice, listed in order of least to most sensitive to epidermal carcinogenesis by initiation and promotion protocols, were found to be equally competent to reactivate herpes simplex virus type 1 irradiated by germicidal UV radiation. Nontumorigenic BALB/c epidermal cell lines selected in vitro for resistance to terminal differentiation after in vivo or in vitro treatment with initiating doses of carcinogens showed virus survival curves similar to those of primary cells. Similarly, primary cultures which were allowed to grow to confluency following a single treatment with the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (100 ng/ml) retained normal host cell reactivation. Host cell reactivation studies with mouse dermal fibroblasts could not be done because of the failure of the herpes simplex virus to infect these cells and produce plaques. Survival of UV light-damaged virus in primary epidermal cells in culture is unrelated to whether the cells are derived from mice sensitive or resistant to epidermal carcinogenesis. Virus survival is not changed by tumor promoter treatment or by treatment with initiating doses of carcinogens which results in differentiation-resistant cells.