MODULATION OF HPV-18 AND BPV-1 TRANSCRIPTION IN HUMAN KERATINOCYTES BY SIMIAN VIRUS-40 LARGE T-ANTIGEN AND ADENOVIRUS TYPE-5 E1A-ANTIGEN

Transcription of early open reading frames initiated from the long control region (LCR) of HPV18 and BPV1 is known to be modulated by homologous and heterologous papillomavirus E2 gene products. Using CAT constructs transfected into normal human keratinocytes, we show that SV40 large T antigen activates transcription from the LCR of both viruses, whereas Ad5‐Ela antigen represses transcription from the HPV18‐LCR but activates transcription from BPVI‐LCR. Experiments using constructs containing subfragments of the HPV18‐LCR cloned in enhancer configuration ahead of the SV40 early promoter or the HSVI‐Tk promoter suggest that the effect of Ad5‐Ela antigen on HPV18 transcription is probably due to a repression of the enhancer function of the LCR. The mechanism of transcription stimulation by SV40 large T antigen is less clear. The 230 bp Rsal‐Rsal central domain of the HPV18‐LCR seems involved both in transcriptional stimulation by SV40 large T antigen and transcriptional inhibition by adenovirus Ela antigen. Copyright © 1990 Wiley‐Liss, Inc.