The role of EBV in haematolymphoid proliferations: emerging concepts relevant to diagnosis and treatment

Epstein–Barr virus (EBV) is a ubiquitous gammaherpesvirus with >90% of the adult population worldwide harbouring latent infection. A small subset of those infected develop EBV‐associated neoplasms, including a range of lymphoproliferative disorders (LPD). The diagnostic distinction of these entit...

Full description

Saved in:
Bibliographic Details
Published in:Histopathology 2021-10, Vol.79 (4), p.451-464
Main Authors: Ababneh, Emad, Saad, Anas M, Crane, Genevieve M
Format: Article
Language:English
Subjects:
Burkitt lymphoma
cancer metabolism
Deoxyribonucleic acid
Diagnosis
DNA
Epstein-Barr virus
Epstein-Barr Virus Infections - complications
Gene expression
Humans
Immune response
Immunogenicity
Immunoproliferative diseases
immunosuppression
Immunosurveillance
Latency
Latent infection
Lymphocytes
lymphoma
lymphoproliferative disorder
Lymphoproliferative Disorders - diagnosis
Lymphoproliferative Disorders - therapy
Lymphoproliferative Disorders - virology
Medical diagnosis
Microenvironments
Tumors
viral metabolomics
Virions
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Epstein–Barr virus (EBV) is a ubiquitous gammaherpesvirus with >90% of the adult population worldwide harbouring latent infection. A small subset of those infected develop EBV‐associated neoplasms, including a range of lymphoproliferative disorders (LPD). The diagnostic distinction of these entities appears increasingly relevant as our understanding of EBV–host interactions and mechanisms of EBV‐driven lymphomagenesis improves. EBV may lower the mutational threshold for malignant transformation, create potential vulnerabilities related to viral alteration of cell metabolism and allow for improved immune targeting. However, these tumours may escape immune surveillance by affecting their immune microenvironment, limiting viral gene expression or potential loss of the viral episome. Methods to manipulate the latency state of the virus to enhance immunogenicity are emerging as well as the potential to detect so‐called ‘hit and run’ cases where EBV has been lost. Finally, measurement of EBV DNA remains an important biomarker for screening and monitoring of LPD. Methods to distinguish EBV DNA derived from virions during lytic activation from latent, methylated EBV DNA present in EBV‐associated neoplasms may broaden the utility of this testing, particularly in patients with compromised immune function. We highlight some of these emerging areas relevant to the diagnosis and treatment of EBV‐associated LPD with potential applicability to other EBV‐associated neoplasms.
ISSN:0309-0167
1365-2559
DOI:10.1111/his.14379