Elevated expression of c-myc in lymphoblastoid cells does not support an Epstein–Barr virus latency III-to-I switch

A Pajic, A Polack, MS Staege… - Journal of General …, 2001 - microbiologyresearch.org
A Pajic, A Polack, MS Staege, D Spitkovsky, B Baier, GW Bornkamm, G Laux
Journal of General Virology, 2001microbiologyresearch.org
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 …
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.
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