@article{mbs:/content/journal/jgv/10.1099/0022-1317-82-12-3051, author = "Pajic, Alexander and Polack, Axel and Staege, Martin S. and Spitkovsky, Dimitry and Baier, Barbara and Bornkamm, Georg W. and Laux, Gerhard", title = "Elevated expression of c-myc in lymphoblastoid cells does not support an Epstein–Barr virus latency III-to-I switch", journal= "Journal of General Virology", year = "2001", volume = "82", number = "12", pages = "3051-3055", doi = "https://doi.org/10.1099/0022-1317-82-12-3051", url = "https://www.microbiologyresearch.org/content/journal/jgv/10.1099/0022-1317-82-12-3051", publisher = "Microbiology Society", issn = "1465-2099", type = "Journal Article", abstract = "Epstein–Barr virus (EBV) transforms primary B cells in vitro. Established cell lines adopt a lymphoblastoid phenotype (LCL). In contrast, EBV-positive Burkitt’s lymphoma (BL) cells, in which the proto-oncogene c-myc is constitutively activated, do not express a lymphoblastoid phenotype in vivo. The two different phenotypes are paralleled by two distinct programmes of EBV latent gene expression termed latency type I in BL cells and type III in LCL. Human B cell lines were established from a conditional LCL (EREB2-5) by overexpression of c-myc and inactivation of EBV nuclear protein 2 (EBNA2). These cells (A1 and P493-6) adopted a BL phenotype in the absence of EBNA2. However, the EBV latency I promoter Qp was not activated. Instead, the latency III promoter Cp remained active. These data suggest that the induction of a BL phenotype by overexpression of c-myc in an LCL is not necessarily paralleled by an EBV latency III-to-I switch.", }