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An Epstein-Barr Virus Anti-Apoptotic Protein Constitutively Expressed in Transformed Cells and Implicated in Burkitt Lymphomagenesis: The Wp/BHRF1 Link 1 1 1 1 1 Gemma L. Kelly , Heather M. Long , Julianna Stylianou , Wendy A. Thomas , Alison Leese , Andrew I. 1 2 3 1 1 Bell , Georg W. Bornkamm , Josef Mautner , Alan B. Rickinson *, Martin Rowe 1 Cancer Research UK Institute for Cancer Studies, The University of Birmingham, Edgbaston, Birmingham, United Kingdom, 2 GSF-Institut fur Klinische Molekularbiologie und Tumorgenetik GSF-Forschungszentrum fur Umwelt und Gesundheit, Munich, Germany, 3 Munich University of Technology, Children’s Hospital, Munich, Germany Abstract Two factors contribute to Burkitt lymphoma (BL) pathogenesis, a chromosomal translocation leading to c-myc oncogene deregulation and infection with Epstein-Barr virus (EBV). Although the virus has B cell growth–transforming ability, this may not relate to its role in BL since many of the transforming proteins are not expressed in the tumor. Mounting evidence supports an alternative role, whereby EBV counteracts the high apoptotic sensitivity inherent to the c-myc–driven growth program. In that regard, a subset of BLs carry virus mutants in a novel form of latent infection that provides unusually strong resistance to apoptosis. Uniquely, these virus mutants use Wp (a viral promoter normally activated early in B cell transformation) and express a broader-than-usual range of latent antigens. Here, using an inducible system to express the candidate antigens, we show that this marked apoptosis resistance is mediated not by one of the extended range of EBNAs