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UV‐ENHANCED VIRUS REACTIVATION IN MAMMALIAN CELLS: EFFECTS OF METABOLIC INHIBITORS*
Author(s) -
Lytle C. D.,
Goddard J. G.
Publication year - 1979
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/j.1751-1097.1979.tb07798.x
Subject(s) - cycloheximide , virus , protein biosynthesis , dna synthesis , biology , herpes simplex virus , cell culture , protein synthesis inhibitor , dna , virology , microbiology and biotechnology , cell , biochemistry , genetics
—The induction process of UV‐enhanced reactivation of UV‐irradiated herpes simplex virus was investigated in CV‐1 monkey kidney cells. A protein synthesis inhibitor, cycloheximide (0.5–5 μg/m/), present in the culture medium For 24 h between cell irradiation and virus infection decreased the enhanced virus survival normally found in UV‐irradiated cultures. The enhanced virus reactivation became essentially resistant to the addition of cycloheximide by 6–8 h after cell irradiation, indicating that the cycloheximide‐sensitive process necessary for enhanced reactivation was complete by that time. Since cycloheximide not only inhibits protein synthesis, but DNA synthesis as well, we investigated the effect of a DNA synthesis inhibitor, hydroxyurea. Hydroxyurea did not decrease UV‐enhanced virus survival, but resulted in enhanced virus survival even in unirradiated cells. Therefore, the cycloheximide‐caused inhibition of UV‐enhanced reactivation did not arise from inhibition of DNA synthesis. The combined results indicate that (1) UV‐enhanced virus reactivation in monkey kidney cells requires de novo protein synthesis during the first 6–8 h after cell irradiation and that (2) DNA synthesis inhibition may be the initiating event.