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Journal of Virology, October 2002, p. 10427-10436, Vol. 76, No. 20
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.20.10427-10436.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Epstein-Barr Virus-Induced Changes in B-Lymphocyte Gene Expression

Kara L. Carter,{dagger} Ellen Cahir-McFarland, and Elliott Kieff*

Departments of Medicine and Microbiology and Molecular Genetics, Harvard Medical School, and The Channing Laboratory, Brigham and Women's Hospital, Boston, Massachusetts 02115

Received 14 February 2002/ Accepted 15 July 2002

To elucidate the mechanisms by which Epstein-Barr virus (EBV) latency III gene expression transforms primary B lymphocytes to lymphoblastoid cell lines (LCLs), the associated alterations in cell gene expression were assessed by using 4,146 cellular cDNAs arrayed on nitrocellulose filters and real-time reverse transcription-PCR (RT-PCR). A total of 1,405 of the 4,146 cDNAs were detected using cDNA probes from poly(A)+ RNA of IB4 LCLs, a non-EBV-infected Burkitt's lymphoma (BL) cell line, BL41, or EBV latency III-converted BL41 cells (BL41EBV). Thirty-eight RNAs were consistently twofold more abundant in the IB4 LCL and BL41EBV than in BL41 by microarray analysis. Ten of these are known to be EBV induced. A total of 23 of 28 newly identified EBV-induced genes were confirmed by real-time RT-PCR. In addition, nine newly identified genes and CD10 were EBV repressed. These EBV-regulated genes encode proteins involved in signal transduction, transcription, protein biosynthesis and degradation, and cell motility, shape, or adhesion. Seven of seven newly identified EBV-induced RNAs were more abundant in newly established LCLs than in resting B lymphocytes. Surveys of eight promoters of newly identified genes implicate NF-{kappa}B or PU.1 as potentially important mediators of EBV-induced effects through LMP1 or EBNA2, respectively. Thus, examination of the transcriptional effects of EBV infection can elucidate the molecular mechanisms by which EBV latency III alters B lymphocytes.

* Corresponding author. Mailing address: The Channing Laboratory, Brigham and Women's Hospital, 181 Longwood Ave., Boston, MA 02115. Phone: (617) 525-4252. Fax: (617) 525-4257. E-mail: ekieff{at}rics.bwh.harvard.edu.

{dagger} Present address: Praecis Pharmaceuticals Incorporated, Waltham, MA 02451.

Journal of Virology, October 2002, p. 10427-10436, Vol. 76, No. 20
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.20.10427-10436.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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