RADIATION ENHANCED REACTIVATION OF NUCLEAR REPLICATING MAMMALIAN VIRUSES*

Abstract

Abstract— When CV‐1 monkey kidney cells were UV‐irradiated (0–18 J/m2) or X‐irradiated (0–10krads) before infection with UV‐irradiated simian adenovirus 7 (SA7) or simian virus 40 (SV40), increases in the infectivity of these nuclear replicating viruses as measured by plaque formation were observed. These radiation enhanced reactivations, UV enhanced reactivation (UVER) and X‐ray enhanced reactivation (X‐ray ER), occurred both when virus infection immediately followed irradiation of the cells (except for X‐ray ER with SA7) and when virus infection was delayed until 3–5 days after cell irradiation. While there was little difference in the levels of reactivation of UV‐irradiated SV40 between immediate and delayed infection, delayed infection resulted in higher levels of reactivation of SA7. X‐ray enhanced reactivation of UV‐irradiated Herpes simplex virus persisted for several days but did not increase. Thus, X‐ray enhanced and UV enhanced reactivations of these mammalian viruses were relatively long‐lived effects. Essentially no UVER or X‐ray ER was found in CV‐1 cells for either immediate or delayed infection with UV‐irradiated vaccinia virus or poliovirus, both of which replicate in the cell cytoplasm. These results suggest UVER and X‐ray ER in mammalian cells may be restricted to viruses which are replicated in the cell nucleus.