TY - JOUR
T1 - Heat-shock-induced enhanced reactivation of UV-irradiated Herpesvirus
AU - Yager, James D.
AU - Zurlo, Joanne
AU - Penn, Arthur L.
N1 - Funding Information:
Joanne Zurlo and was carried out while Joanne Zurlo and James D. Yager were in the Department of Environmental Medicine, New York University Medical Center, 550 First Avenue, New York, NY 10016. James D. Yager and Arthur L. Penn received support from PHS grant ES00260 awarded to the Institute of Environmental Medicine. The authors wish to thank Drs. E. Berger and E. Pfefferkorn (Dartmouth) for their critical comments on the manuscript, K. Bracco and L. Batta (NYU) for excellent technical assistance, K. Baumgartner (Darmouth) for assistance with the statistical analysis and J. Vance (Dartmouth) for help in preparing the manuscript.
Copyright:
Copyright 2014 Elsevier B.V., All rights reserved.
PY - 1985/9
Y1 - 1985/9
N2 - The objective of this study was to compare the ability of heat stock (HS) with that of another type of cellular stress, UV irradiation, to cause the induction of enhanced viral reactivation, a process that may represent an SOS-type repair process in mammalian cells. Studies performed to evaluate the effect of HS on growth of Vero cells revealed that HS at 45°C for 45 min caused inhibition of cell growth similar to that caused by UV irradiation at 12 J/m2, but this inhibition was not observed at HS treatment for 5-15 min, or at a UV fluence of 2 J/m2. Enhanced reactivation of UV-irradiated Herpesvierus was observed in cells which had been pretreated by HS for > 30 min or UV at 12 J/m2. The synthesis of new proteins following HS for 15 and 45 min and UV at 12 J/m2 was examined by [35S]methionine-labeling experiments. The new synthesis of two HS proteins with molecular weights of 46 000 and 78 000 was induced by both levels of HS, but to a much greater extent at the high dose. These proteins were not detected in response to UV irradiation. These results indicate that, like UV irradiation, HS at levels inhibitory to cell growth induced enhanced viral reactivation in Vero cells. The results also suggest that at least two proteins in the HS protein family are not necessary for this response to occur.
AB - The objective of this study was to compare the ability of heat stock (HS) with that of another type of cellular stress, UV irradiation, to cause the induction of enhanced viral reactivation, a process that may represent an SOS-type repair process in mammalian cells. Studies performed to evaluate the effect of HS on growth of Vero cells revealed that HS at 45°C for 45 min caused inhibition of cell growth similar to that caused by UV irradiation at 12 J/m2, but this inhibition was not observed at HS treatment for 5-15 min, or at a UV fluence of 2 J/m2. Enhanced reactivation of UV-irradiated Herpesvierus was observed in cells which had been pretreated by HS for > 30 min or UV at 12 J/m2. The synthesis of new proteins following HS for 15 and 45 min and UV at 12 J/m2 was examined by [35S]methionine-labeling experiments. The new synthesis of two HS proteins with molecular weights of 46 000 and 78 000 was induced by both levels of HS, but to a much greater extent at the high dose. These proteins were not detected in response to UV irradiation. These results indicate that, like UV irradiation, HS at levels inhibitory to cell growth induced enhanced viral reactivation in Vero cells. The results also suggest that at least two proteins in the HS protein family are not necessary for this response to occur.
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U2 - 10.1016/0167-8817(85)90001-X
DO - 10.1016/0167-8817(85)90001-X
M3 - Article
C2 - 2993875
AN - SCOPUS:0022390664
SN - 0167-8817
VL - 146
SP - 121
EP - 128
JO - Mutation Research DNA Repair Reports
JF - Mutation Research DNA Repair Reports
IS - 2
ER -