Abstract
Here, we wish to highlight the genetic exchange and epigenetic interactions between Epstein–Barr virus (EBV) and its host. EBV is associated with diverse lymphoid and epithelial malignancies. Their molecular pathogenesis is accompanied by epigenetic alterations which are distinct for each of them. While lymphoblastoid cell lines derived from B cells transformed by EBV in vitro are characterized by a massive demethylation and euchromatinization of the viral and cellular genomes, the primarily malignant lymphoid tumor Burkitt’s lymphoma and the epithelial tumors nasopharyngeal carcinoma and EBV-associated gastric carcinoma are characterized by hypermethylation of a multitude of cellular tumor suppressor gene loci and of the viral genomes. In some cases, the viral latency and oncoproteins including the latent membrane proteins LMP1 and LMP2A and several nuclear antigens affect the level of cellular DNA methyltransferases or interact with the histone modifying machinery. Specific molecular mechanisms of the epigenetic dialog between virus and host cell remain to be elucidated.
Highlights
EPSTEIN–BARR VIRUS—THE FIRST HUMAN TUMOR VIRUS Epstein–Barr virus (EBV), the proto-typical gamma-herpesvirus infecting humans, has been discovered 50 years ago in cultured Burkitt’s lymphoma (BL) cells (Epstein et al, 1964)
General view was that the EBV-transformed cell was the origin of the endemic BL cell, too, a fundamental difference of the epidemiology and pathogenesis between lymphoblastoid cell line (LCL)-like tumors on one side, and of primarily malignant EBV-associated lymphomas www.frontiersin.org
Onset post-transplant lymphoproliferative disorder (PTLD) originate under conditions of severe immune suppression and depend on viral transforming functions, including EBV nuclear antigens (EBNAs) and latent membrane proteins (LMPs) that are expressed both in PTLDs in vivo and in LCLs immortalized in vitro
Summary
EPSTEIN–BARR VIRUS—THE FIRST HUMAN TUMOR VIRUS Epstein–Barr virus (EBV), the proto-typical gamma-herpesvirus infecting humans, has been discovered 50 years ago in cultured Burkitt’s lymphoma (BL) cells (Epstein et al, 1964). Key viral latency proteins or so-called oncoproteins are differentially expressed in EBV-associated malignancies and transformed cell lines.
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