The LCR of EBV makes Burkitt's lymphoma endemic.
The spectacular ability of Epstein-Barr virus (EBV) to immortalize and morphologically transform human B cells in vitro to lymphoblastoid cell lines (LCLs) is central to most molecular models of viral oncogenesis. However, binding of transcription factor and oncoprotein c-Myc to the major locus control region (LCR) of the viral genome directs us to an alternative model for the origin of Burkitt's lymphoma (BL). In this model, improved nuclear maintenance of the viral genome and the continuous expression of anti-apoptotic functions in B cells exhibiting class I EBV latency contribute to the generation of BL, without any detour through EBV nuclear antigen (EBNA) 2-driven B-cell immortalization (also called class III latency).
Niller
Hans H
HH
Institute for Medical Microbiology and Hygiene, University of Regensburg, Research Center, Landshuter Strasse 22, D-93047 Regensburg, Germany. Hans-Helmut.Niller@klinik.uni-regensburg.de
Salamon
Daniel
D
Banati
Ferenc
F
Schwarzmann
Fritz
F
Wolf
Hans
H
Minarovits
Janos
J
D017209:Apoptosis; D001402:B-Lymphocytes / Q000166:cytology / Q000821:virology; D002051:Burkitt Lymphoma / Q000821:virology*; D002470:Cell Survival; D004854:Herpesvirus 4, Human / Q000235:genetics* / Q000472:pathogenicity*; D006801:Humans; D019901:Locus Control Region; D016271:Proto-Oncogene Proteins c-myc / Q000378:metabolism*; D017735:Virus Latency
C489427:MYC protein, human; D016271:Proto-Oncogene Proteins c-myc