This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lucchesi, W.
Right arrow Articles by Farrell, P. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lucchesi, W.
Right arrow Articles by Farrell, P. J.

 Previous Article  |  Next Article 

Journal of Virology, August 2008, p. 7456-7466, Vol. 82, No. 15
0022-538X/08/$08.00+0     doi:10.1128/JVI.00223-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Differential Gene Regulation by Epstein-Barr Virus Type 1 and Type 2 EBNA2{triangledown}

Walter Lucchesi,1 Gareth Brady,1 Oliver Dittrich-Breiholz,2 Michael Kracht,3 Rainer Russ,4 and Paul J. Farrell1*

Department of Virology, Faculty of Medicine, Imperial College London, Norfolk Place, London W2 1PG, United Kingdom,1 Institute of Biochemistry, Medical School Hannover, Carl-Neuberg Strasse 1, D-30625 Hannover, Germany,2 Rudolf-Buchheim-Institut für Pharmakologie, Frankfurter Strasse 107, D-35392 Giessen, Germany,3 Genedata AG, Maulbeerstrasse 46, CH-4058 Basel, Switzerland4

Received 1 February 2008/ Accepted 7 May 2008

A transfection assay with a lymphoblastoid cell line infected with Epstein-Barr virus was used to compare the abilities of type 1 and type 2 EBNA2 to sustain cell proliferation. The reduced proliferation in cells expressing type 2 EBNA2 correlated with loss of expression of some cell genes that are known to be targets of type 1 EBNA2. Microarray analysis of EBNA2 target genes identified a small number of genes that are more strongly induced by type 1 than by type 2 EBNA2, and one of these genes (CXCR7) was shown to be required for proliferation of lymphoblastoid cell lines. The Epstein-Barr virus LMP1 gene was also more strongly induced by type 1 EBNA2 than by type 2, but this effect was transient. Type 1 and type 2 EBNA2 were equally effective at arresting cell proliferation of Burkitt's lymphoma cell lines lacking Epstein-Barr virus and were also shown to cause apoptosis in these cells. The results indicate that differential gene regulation by Epstein-Barr virus type 1 and type 2 EBNA2 may be the basis for the much weaker B-cell transformation activity of type 2 Epstein-Barr virus strains compared to type 1 strains.

* Corresponding author. Mailing address: Department of Virology, Faculty of Medicine, Imperial College London, St. Mary's Campus, Norfolk Place, London W2 1PG, United Kingdom. Phone: 44 20 7594 2005. Fax: 44 20 7594 3973. E-mail: p.farrell{at}imperial.ac.uk

{triangledown} Published ahead of print on 14 May 2008.

Journal of Virology, August 2008, p. 7456-7466, Vol. 82, No. 15
0022-538X/08/$08.00+0     doi:10.1128/JVI.00223-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Brady, G., Whiteman, H. J., Spender, L. C., Farrell, P. J. (2009). Downregulation of RUNX1 by RUNX3 Requires the RUNX3 VWRPY Sequence and Is Essential for Epstein-Barr Virus-Driven B-Cell Proliferation. J. Virol. 83: 6909-6916 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»