Abstract
Summary
The repair phenomena of host-cell reactivation (HCR), uv reactivation (UVR) and X-ray reactivation (X-ray R) were studied in normal embryonic (OMRE) and malignant (RMT) rat cells of the same strain by examining the survival of uvirradiated herpes simplex virus (HV-1). Experiments indicated that HCR was present to the same extent in both OMRE and RMT cells as evidenced by similar e -1 values for both components of the virus survival curve as well as similar extrapolation numbers for the resistant component. UVR and X-ray R were demonstrated in RMT cells as indicated by enhanced survival of irradiated virus; however, both of these repair processes were absent in OMRE cells. The amount of UVR in RMT cells increased with virus uv dose and cell uv exposure. It was evident that HCR and radiation enhanced reactivation (UVR and X-ray R) may operate independently in these mammalian virus–host cell systems.
We thank Lynda Kramer and Wah Lee for assistance in X-irradiation of cells and C. David Lytle, F. Alan Andersen, and Thomas J. Withrow for helpful discussions and critical review of the manuscript.
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