No abstract

Previous studies have shown that cellular stress agents such as UV radiation induce transcription from the long terminal repeat (LTR) of the human immunodeficiency virus (HIV). Using HeLa cells stably transfected with the HIV-LTR sequence, which transcriptionally drives the chloramphenicol acetyl transferase (CAT) reporter gene, we examined the effects of multiple exposures to UVC (254 nm) on HIV-LTR-CAT expression. Low doses (< or = 5 J m-2) had no effect on CAT expression, but up to 29-fold induction was observed with 10 J m-2 when cells were harvested 48 h after completion of the exposure. Little difference was noted in induction levels when cells were exposed to one 25 J m-2 dose, viable cells were harvested at 24 h, 48 h or 72 h, and cell lysates were assayed for CAT expression. Two sequential 12.5 J m-2 exposures, given 24 h apart, resulted in an additive effect on CAT expression; these two exposures produced CAT activity equivalent to that induced following a single 25 J m-2 dose. This additive effect was not evident at the lower doses (< or = 5 J m-2) or at the higher doses. Maximal induction was observed using doses from 25 to 37.5 J m-2. Multiple exposures with either the low (< or = 5 J m-2) or high doses (> 25 J m-2) did not result in an additive effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Sequences of four of these genes contained NF-kappaB DNA binding sites of the type that may attract transrepressor p55/p55 NF-kappaB homodimers. Down-regulation of these genes upon UV irradiation may contribute to increased cell survival via suppression of p53 independent apoptosis.