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The CR4 region of EBNA2 confers viability of Epstein–Barr virus-transformed B cells by CBF1-independent signalling

Kristina Grabusic^1,

¹ GSF – National Research Center for Environment and Health, Institute of Clinical Molecular Biology, Marchioninistr. 25, D-81377 Munich, Germany
² Department of Gene Vectors, Marchioninistr. 25, D-81377 Munich, Germany

Correspondence
Bettina Kempkes
kempkes{at}gsf.de

The Epstein–Barr virus (EBV) nuclear antigen 2 (EBNA2) gene product is the key regulator of the latent genes of EBV and essential for EBV-mediated transformation of human primary B cells. Viral mutants were constructed carrying a deletion of the EBNA2 conserved region 4 (CR4). Primary resting B cells infected with the CR4-EBNA2 mutant virus were dramatically impaired for B cell transformation. Lymphoblastoid cell lines (LCLs) established with this mutant EBV revealed a prolonged population doubling time when cells were cultivated at low cell densities, which are not critical for wild-type-infected cells. Low-level spontaneous cell death occurred when the cells were cultivated at suboptimal cell densities. The phenotype of B cells and LCLs infected with the CR4-EBNA2 mutant virus indicated that the CR4 region of EBNA2 specifically contributes to the viability of the cells rather than affecting cell division rates.

Present address: University of Rijeka, School of Medicine, Department of Molecular Medicine and Biotechnology, Brace Branchetta 20, 51000 Rijeka, Croatia.

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