Abstract
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 reserves the lethal disruption of an essential function peculiar to the viral early genes region. This function is almost certainly transcription.
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