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Photochem Photobiol 1979 May;29(5):959-62

UV-enhanced virus reactivation in mammalian cells: effects of metabolic inhibitors.

Lytle CD, Goddard JG

Abstract

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 ¿g/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.


Category: Journal Article
PubMed ID: #231792 DOI: 10.1111/j.1751-1097.1979.tb07798.x
Includes FDA Authors from Scientific Area(s): Medical Devices
Entry Created: 2012-12-04
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