UV-enhanced reactivation of UV-damaged SV40 is due to the restoration of viral early gene function.
Mammalian cells respond to UV-radiation by inducing an increased ability to support the survival of UV-damaged virus. We have tested whether the induction of enhanced viral reactivation (ER) reflects heightened UV-resistance of specific viral functions. For this, we examined the extent of ER for SV40 containing UV-damage in three functionally distinct regions of the SV40 genome: (i) the viral regulatory region, (ii) the early genes region and (iii) the late genes region. ER corresponding to a dose reduction factor of 43% was observed for damage in the early genes region. No ER was observed for damage in the regulatory or late genes regions. We conclude that ER in SV40 reverses the lethal disruption of an essential function peculiar to the viral early genes region. This function is almost certainly transcription.
Brown
T C
TC
Swiss Institute for Experimental Cancer Research, Epalinges.
Cerutti
P A
PA
D000818:Animals; D002478:Cells, Cultured; D004279:DNA, Viral / Q000096:biosynthesis / Q000528:radiation effects; D005814:Genes, Viral / Q000528:radiation effects*; D012367:RNA, Viral / Q000096:biosynthesis / Q000235:genetics; D013539:Simian virus 40 / Q000235:genetics / Q000254:growth & development / Q000528:radiation effects*; D014162:Transfection; D014466:Ultraviolet Rays; D010948:Viral Plaque Assay; D014775:Virus Activation / Q000235:genetics / Q000528:radiation effects*
D004279:DNA, Viral; D012367:RNA, Viral