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Journal of Virology, January 1999, p. 826-833, Vol. 73, No. 1
Division of Molecular Virology, Baylor
College of Medicine, Houston, Texas 77030,1 and
Sealy Center for Oncology and Hematology and Division of
Infectious Diseases, Department of Internal Medicine, University of
Texas Medical Branch, Galveston, Texas
77555-10482
Received 10 August 1998/Accepted 7 October 1998
The Epstein-Barr virus (EBV) EBNA2 protein is a transcriptional
activator that controls viral latent gene expression and is essential
for EBV-driven B-cell immortalization. EBNA2 is expressed from the
viral C promoter (Cp) and regulates its own expression by
activating Cp through interaction with the cellular DNA binding protein CBF1. Through regulation of Cp and EBNA2 expression, EBV controls the pattern of latent protein expression and the type of
latency established. To gain further insight into the important regulatory elements that modulate Cp usage, we isolated and sequenced the Cp regions corresponding to nucleotides 10251 to 11479 of the EBV
genome (
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Transcriptional Activation Signals Found in the Epstein-Barr
Virus (EBV) Latency C Promoter Are Conserved in the Latency C
Promoter Sequences from Baboon and Rhesus Monkey EBV-Like
Lymphocryptoviruses (Cercopithicine Herpesviruses 12 and
15)
1079 to +144 relative to the transcription initiation site)
from the EBV-like lymphocryptoviruses found in baboons (herpesvirus papio; HVP) and Rhesus macaques (RhEBV). Sequence comparison of the
approximately 1,230-bp Cp regions from these primate viruses revealed
that EBV and HVP Cp sequences are 64% conserved, EBV and RhEBV Cp
sequences are 66% conserved, and HVP and RhEBV Cp sequences are 65%
conserved relative to each other. Approximately 50% of the residues
are conserved among all three sequences, yet all three viruses have
retained response elements for glucocorticoids, two positionally
conserved CCAAT boxes, and positionally conserved TATA boxes. The
putative EBNA2 100-bp enhancers within these promoters contain 54 conserved residues, and the binding sites for CBF1 and CBF2 are well
conserved. Cp usage in the HVP- and RhEBV-transformed cell lines was
detected by S1 nuclease protection analysis. Transient-transfection analysis showed that promoters of both HVP and RhEBV are responsive to
EBNA2 and that they bind CBF1 and CBF2 in gel mobility shift assays.
These results suggest that similar mechanisms for regulation of latent
gene expression are conserved among the EBV-related lymphocryptoviruses
found in nonhuman primates.
*
Corresponding author. Mailing address: Division of
Molecular Virology, Baylor College of Medicine, One Baylor Plaza,
Houston, TX 77030. Phone: (713) 798-8474. Fax: (713)
798-3586. E-mail: pling{at}bcm.tmc.edu.
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