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

This Article Figures Only Full Text Full Text (PDF) Correspondence: Submit a response Alert me when this article is cited Alert me when Correspondence are posted 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 Google Scholar Google Scholar Articles by Meier, J. L. Articles by Straus, S. E. Search for Related Content PubMed PubMed Citation Articles by Meier, J. L. Articles by Straus, S. E.

Interactions between varicella-zoster virus IE62 and cellular transcription factor USF in the coordinate activation of genes 28 and 29

From the Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD.
Address correspondence and reprint requests to Dr. Stephen E. Straus at the Laboratory of Clinical Investigation, Building 10, Room 11N228, NIH, Bethesda, MD 20892-1888.

Varicella-zoster virus (VZV) gene 28 encodes the viral DNA polymerase, while 29 encodes the major DNA-binding protein. Because of the central importance of these proteins to productive replication of VZV and because, of these, only gene 29 seems to be expressed in latency, we sought to understand how their expression is controlled. We recently reported that the divergent gene 28 and gene 29 transcripts are coordinately upregulated by IE62. Deletions in the 221-bp promoter domain shared by genes 28 and 29 comparably diminish the expression of both genes. By a variety of transient expression, competition gel shift, and super-shift assays, we now show that cellular transcription factor USF binds to a palindromic recognition sequence lying equidistant from transcription start sites for both genes 28 and 29. In the presence of IE62, USF fully activates transcription of genes 28 and 29. Site-specific mutation of three bases in the USF core binding hexamer abrogates activation of the gene 28 and 29 promoters by IE62. USF is important for expression of genes 28 and 29 in productive VZV infection.

NEUROLOGY 1995;45(Suppl 8): S30-S32