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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 p21(WAF1) accumulated in mitogen-stimulated primary B cells following exposure to all genotoxins tested. In contrast, when proliferation was EBV driven, p21(WAF1) 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.

Original publication




Journal article


J virol

Publication Date





12408 - 12413


B-Lymphocytes, Cyclin-Dependent Kinase Inhibitor p21, DNA Damage, Gene Expression Regulation, Herpesvirus 4, Human, Mutagens, Phosphorylation, Tumor Suppressor Protein p53