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Journal of Virology, December 2006, p. 12408-12413, Vol. 80, No. 24
0022-538X/06/$08.00+0     doi:10.1128/JVI.01363-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Epstein-Barr Virus Selectively Deregulates DNA Damage Responses in Normal B Cells but Has No Detectable Effect on Regulation of the Tumor Suppressor p53{triangledown}

Jenny O'Nions, Abigail Turner, Richard Craig, and Martin J. Allday*

Department of Virology, Faculty of Medicine, Imperial College London, Norfolk Place, London W2 1PG, United Kingdom

Received 28 June 2006/ Accepted 8 September 2006

To determine whether latent Epstein-Barr virus (EBV) modifies DNA damage responses in B lymphocytes, cells were treated with agents either producing DNA cross-links and adducts or generating double-strand breaks. The cyclin-dependent kinase inhibitor p21WAF1 accumulated in mitogen-stimulated primary B cells following exposure to all genotoxins tested. In contrast, when proliferation was EBV driven, p21WAF1 failed to accumulate after treatment with the DNA adduct-producing agents. The tumor suppressor p53 was stabilized and phosphorylated after all treatments, irrespective of whether latent EBV was present. This suggests that regulatory pathways upstream of p53 are unaffected by latent EBV but downstream effectors are altered if DNA adducts or distortions are involved.

* Corresponding author. Mailing address: Department of Virology, Faculty of Medicine, Norfolk Place, London W2 1PG, United Kingdom. Phone: 44 (0) 2075943836. Fax: 44 (0) 2075943973. E-mail: m.allday{at}imperial.ac.uk.

{triangledown} Published ahead of print on 20 September 2006.

Journal of Virology, December 2006, p. 12408-12413, Vol. 80, No. 24
0022-538X/06/$08.00+0     doi:10.1128/JVI.01363-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

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