1887

Abstract

Epstein–Barr virus (EBV) transforms primary B cells . Established cell lines adopt a lymphoblastoid phenotype (LCL). In contrast, EBV-positive Burkitt’s lymphoma (BL) cells, in which the proto-oncogene c- is constitutively activated, do not express a lymphoblastoid phenotype . 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 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- in an LCL is not necessarily paralleled by an EBV latency III-to-I switch.

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2001-12-01
2020-01-23
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