HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by May, M. Articles by Fuchs, P. G. Search for Related Content PubMed PubMed Citation Articles by May, M. Articles by Fuchs, P. G. Agricola Articles by May, M. Articles by Fuchs, P. G.

Unique Topography of DNA-protein Interactions in the Non-coding Region of Epidermodysplasia Verruciformis-associated Human Papillomaviruses

Institut für Klinische und Molekulare Virologie der Friedrich-Alexander Universität Erlangen-Nürnberg, Loschgestrasse 7, 8520 Erlangen, Germany

The non-coding region (NCR) of the epidermodysplasia verruciformis (EV)-associated human papillomavirus 8 (HPV-8) has been investigated for sequence-specific DNA-protein interactions with nuclear proteins from epithelial HeLa cells. Using DNase I protection analysis 18 footprints could be found within the HPV-8 NCR, covering altogether over 60% of both DNA strands. Several footprints coincided with the known binding sites of transcription factors (NF1, AP1, octamer and PEA3 consensus sequences); the other displayed no obvious similarities in this regard. The overall distribution of sequences involved in DNA-protein interactions differed clearly from the binding patterns reported for other HPVs. Parts of the two binding sites for the viral trans-activator protein E2 were shown to interact with non-E2 factors. The EV-specific NCR motifs M33, M29 and A/T box were all involved in protein binding. By comparing the footprints within the respective motifs of the closely related types HPV-8 and -19, quantitative and qualitative differences were detected for M33 and the A/T box.

Received 24 June 1991; accepted 26 August 1991.