Epstein-Barr virus (EBV) infection leaves lasting epigenetic imprint

Epstein-Barr virus (EBV) is a prevalent human herpesvirus affecting over
90% of the adult population worldwide. Most individuals harbor EBV
asymptomatically as lifelong infections. However, in rare cases, EBV is
associated with epithelial and B cell malignancies. The viral life cycle
is dependent on host epigenetic machinery to regulate viral gene
expression programs that ensure viral persistence and spread. Infection
with EBV can lead to epigenetic changes in the host cell as well.
Several EBV proteins interact with host epigenetic machinery, such as
the latent membrane proteins ability to induce the activity of the DNA
methyltransferases (DMNT) [1-3]. The consequences of which can best be seen in EBV-associated malignancies with the CpG island methylator phenotype (CIMP) [4, 5].
CIMP is where CpG islands upstream of tumor suppressors are
hypermethylated and this phenotype has a strong correlation with EBV.
Whether EBV directs the DNA methylation changes, or if the epigenetic
changes are due to the carcinogenic process are still being defined.

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