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Burkitt lymphoma: the role of Epstein‐Barr virus revisited
Author(s) -
Grömminger Sebastian,
Mautner Josef,
Bornkamm Georg W.
Publication year - 2012
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.2011.09007.x
Subject(s) - virus , biology , lymphoma , virology , epstein–barr virus , pathogenesis , population , antibody , burkitt's lymphoma , immunology , cancer research , medicine , environmental health
SummaryThe particular epidemiological features of Burkitt lymphoma (BL) in Tropical Africa, first described by Denis Burkitt in 1958, initiated the search for a virus that induces malignant B cell lymphomas in humans and is transmitted by arthropods. The herpes virus (Epstein‐Barr virus, EBV) discovered by Epstein and collaborators in cell lines established from BL biopsies fulfilled some of these predictions. It drives primary B cells into unlimited proliferation, induces malignant B cell lymphomas in immunocompromised individuals (post‐transplant lympho‐proliferative disease, PTLD) in vivo , and footprints of the virus are generally detected in African BL biopsies supporting a causative role of the virus in the pathogenesis of BL. The virus is, however, not transmitted by arthropods and is spread ubiquitously amongst the human population through saliva. Furthermore, BL and EBV‐induced PTLD are now recognized as pathogenetically distinct entities: BL involves MYC ‐immunoglobulin translocations in contrast to PTLD, and different patterns of viral genes are expressed in both diseases. Viral gene products expressed in BL are assumed to contribute to inhibition of apoptosis, although their precise mechanism of action is not fully understood. In the future, next generation sequencing is expected to shed more light on the contribution of EBV to the pathogenesis of BL.