Epstein-Barr virus-associated lymphomas.
Claire Shannon-LoweAlan B RickinsonAndrew I BellPublished in: Philosophical transactions of the Royal Society of London. Series B, Biological sciences (2018)
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'.
Keyphrases
- epstein barr virus
- diffuse large b cell lymphoma
- gene expression
- sars cov
- nk cells
- induced apoptosis
- endothelial cells
- transcription factor
- dna methylation
- cell cycle arrest
- oxidative stress
- endoplasmic reticulum stress
- cell death
- induced pluripotent stem cells
- respiratory failure
- acute respiratory distress syndrome
- disease virus
- mechanical ventilation