Enhanced mutagenesis parallels enhanced reactivation of herpes virus in a human cell line.

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Abstract
U.v. irradiation of human NB‐E cells results in enhanced mutagenesis and enhanced reactivation of u.v.‐irradiated H‐1 virus grown in those cells (Cornelis et al., 1982). This paper reports a similar study using herpes simplex virus (HSV) in NB‐E cells. The mutation frequency of HSV (resistance of virus plaque formation to 40 micrograms/ml iododeoxycytidine) increased approximately linearly with exposure of the virus to u.v. radiation. HSV grown in unirradiated cells gave a slope of 1.8 X 10(‐5)m2/J, with 3.2 X 10(‐5)m2/J for HSV grown in cells irradiated (3 J/m2) 24 h before infection. There was no evidence for mutagenesis of unirradiated virus by irradiated cells, as seen with H‐1 virus. Enhanced reactivation of irradiated HSV in parallel cultures increased virus survival, manifested as a change in slope of the final component of the two‐component survival curve from a D0 of 27 J/m2 in unirradiated cells to 45 J/m2 in irradiated cells. Thus, enhanced mutagenesis and enhanced reactivation occurred for irradiated HSV in NB‐E cells. The difference in the enhanced mutagenesis of HSV (dependent on damaged DNA sites) and of H‐1 virus (primarily independent of damaged DNA sites) is discussed in terms of differences in DNA polymerases.

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