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Journal of Virology, February 2005, p. 1724-1733, Vol. 79, No. 3
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.3.1724-1733.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Regulation of Expression of the Epstein-Barr Virus BamHI-A Rightward Transcripts

Honglin Chen,1 Jian Huang,2,3 Frederick Y. Wu,2 Gangling Liao,2 Lindsey Hutt-Fletcher,4 and S. Diane Hayward2,3*

Department of Microbiology, The University of Hong Kong, Hong Kong,1 Viral Oncology Program, Sidney Kimmel Cancer Center,2 Department of Pharmacology and Molecular Sciences, Johns Hopkins School of Medicine, Baltimore, Maryland,3 Department of Microbiology and Immunology, Louisiana State University Health Sciences Center, Shreveport, Louisiana4

Received 7 July 2004/ Accepted 9 September 2004

The Epstein-Barr virus (EBV) BamHI-A rightward transcripts, or BARTs, are a family of mRNAs expressed in all EBV latency programs, including EBV-infected B cells in healthy carriers. Despite their ubiquitous expression, the regulation and biological function of BARTs are still unclear. In this study, the BART 5' termini were characterized by using a procedure that selects capped, full-length mRNAs. Two TATA-less promoter regions, designated P1 and P2, were mapped. P1 had relatively high basal activity in both epithelial and B cells, whereas P2 exhibited higher activity in epithelial cells. Upon EBV infection of B cells, transcription from P1 was detected soon after infection, while expression from P2 was delayed. Promoter-reporter assays in transiently transfected cells revealed that P1 and P2 were differentially regulated. Interferon regulatory factor 7 (IRF7) and IRF5 negatively regulated P1 activity. c-Myc and C/EBP family members positively regulated P2. Regulation of P2 by C/EBPs was characterized by electrophoretic mobility shift assay, chromatin immunoprecipitation, and reporter assays. More-abundant BART expression in epithelial cells correlated with the relative expression of positive and negative regulators in these cells.

* Corresponding author. Mailing address: Johns Hopkins University School of Medicine, Bunting-Blaustein Building CRB308, 1650 Orleans St., Baltimore, MD 21231-1000. Phone: (410) 614-0592. Fax: (410) 502-6802. E-mail: dhayward{at}jhmi.edu.

Journal of Virology, February 2005, p. 1724-1733, Vol. 79, No. 3
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.3.1724-1733.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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