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Journal of Virology, May 2002, p. 4919-4927, Vol. 76, No. 10
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.10.4919-4927.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Expression of Transcription Factor AML-2 (RUNX3, CBF{alpha}-3) Is Induced by Epstein-Barr Virus EBNA-2 and Correlates with the B-Cell Activation Phenotype

Lindsay C. Spender,1 Georgina H. Cornish,1,{dagger} Alexandra Sullivan,1 and Paul J. Farrell1,2*

Ludwig Institute for Cancer Research,1 Virology and Cell Biology Section, Imperial College Faculty of Medicine, London W2 1PG, United Kingdom2

Received 29 November 2001/ Accepted 4 February 2002

To identify cell proteins regulated by the Epstein-Barr virus (EBV) transcription factor EBNA-2, we analyzed a cell line with conditional EBNA-2 activity by using microarray expression profiling. This led to the identification of two novel target genes induced by EBNA-2. The first of these, interleukin-16, is an immunomodulatory cytokine involved in the regulation of CD4 T cells. The second, AML-2, is a member of the Runt domain family of transcription factors. Quiescent B cells initially expressed AML-1 but, 48 h after virus infection, the levels of AML-1 decreased dramatically, whereas the amount of AML-2 protein increased. Analysis of a panel of B-cell lines indicated that AML-2 expression is normally predominant in EBV latency III, whereas AML-1 is associated with EBV latency I or EBV-negative cells. The AML genes are the first example of cell transcription factors whose expression correlates with the latency I/III phenotype.

* Corresponding author. Mailing address: Ludwig Institute for Cancer Research, Imperial College Faculty of Medicine, Norfolk Place, London W2 1PG, United Kingdom. Phone: 44-20-7563-7703. Fax: 44-20-7724-8586. E-mail: p.farrell{at}ic.ac.uk.

{dagger} Present address: ICRF, London WC2A 3PX, United Kingdom.

Journal of Virology, May 2002, p. 4919-4927, Vol. 76, No. 10
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.10.4919-4927.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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