Epstein–Barr virus-associated lymphomas. (11th September 2017)

• Record Type: Journal Article
• Authors: Shannon-Lowe, Claire; Rickinson, Alan B.; Bell, Andrew I.
• Is Part Of: Philosophical transactions. Volume 372:Number 1732(2017)
• Publication Date: 2017-09-11
• Subjects: Epstein–Barr virus -- Burkitt lymphoma -- Hodgkin lymphoma -- post-transplant lymphoproliferative disease -- diffuse large B cell lymphoma -- T/NK lymphoma; Biology -- Periodicals; Science -- Periodicals; 570
• DOI: 10.1098/rstb.2016.0271
• Languages: English
• ISSNs: 0962-8436

Abstract

Abstract : Epstein–Barr virus (EBV), originally discovered through its association with Burkitt lymphoma, is now aetiologically linked to a remarkably wide range of lymphoproliferative lesions and malignant lymphomas of B-, T- and NK-cell origin. Some occur as rare accidents of virus persistence in the B lymphoid system, while others arise as a result of viral entry into unnatural target cells. The early finding that EBV is a potent B-cell growth transforming agent hinted at a simple oncogenic mechanism by which this virus could promote lymphomagenesis. In reality, the pathogenesis of EBV-associated lymphomas involves a complex interplay between different patterns of viral gene expression and cellular genetic changes. Here we review recent developments in our understanding of EBV-associated lymphomagenesis in both the immunocompetent and immunocompromised host. This article is part of the themed issue 'Human oncogenic viruses'.