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’.
Highlights
Epstein–Barr virus infection, virus-induced lymphoproliferative diseases and the virus-associated lymphomasEpstein –Barr virus (EBV), a human gamma-1 herpesvirus, is widespread in all populations and is carried as a latent asymptomatic infection in the vast majority of individuals
Some primary EBV infections are clinically manifest as infectious mononucleosis (IM), a febrile illness characterized by hyper-expansion of both lytic and latent antigenspecific T cell responses, while lower levels of these same responses persist as memory T cells in the blood of all virus carriers and are enriched as tissue-resident populations in oropharyngeal lymphoid tissues where EBV reactivations are thought to initiate [4,5]
EBL and sporadic BL (sBL) differ in the detailed anatomy of Ig/c-MYC breakpoints [52], in the frequency and pattern of Ig mutations [53] and in their gene expression profiles [54], implying that EBV-positive and negative forms of the disease may originate from germinal centre (GC) B cells at subtly distinct stages of maturation
Summary
Epstein–Barr virus infection, virus-induced lymphoproliferative diseases and the virus-associated lymphomas. Epstein –Barr virus (EBV), a human gamma-1 herpesvirus, is widespread in all populations and is carried as a latent asymptomatic infection in the vast majority of individuals This same agent has powerful lymphocyte growth-transforming ability and is aetiologically linked to a range of lymphoproliferative lesions and malignant lymphomas [1]. EBV does successfully infect and establish persistence in the naive host This very likely reflects the ability of some growth-transformed B cells in vivo to downregulate latent antigen expression and switch to a truly latent resting state, thereby escaping immune detection. In contrast to the acute B-LPDs, the heightened lymphoma risk in these patient groups is not coincident with times of peak T cell impairment and other factors must come into play Besides these B cell diseases, table 1 lists the surprising links between EBV, ostensibly a B-lymphotropic virus, and both lymphoproliferative disease and malignant lymphomas of T or NK cell origin. Gains fortuitous access to the T- and/or NK-cell lineages, with serious consequences for the host as described in the later sections of this review
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