Could Changing the DNA Methylation Landscape Promote the Destruction of Epstein-Barr Virus-Associated Cancers?

DNA methylation at CpG motifs provides an epigenetic route to regulate gene expression. In general, inverse correlation between hypermethylation and expression is observed. Epstein Barr-virus (EBV) infects people the EBV genome resides in nucleus where either its replication cycle initiates or it enters a long-term latency state viral becomes hypermethylated motifs. Viral shows largely with hypermethylation. occurs through action of methyl transferase enzymes: writer transferases add groups specific regions unmethylated DNA; maintenance reproduce pattern during replication. The impact achieved association various proteins specifically methylated their influence on regulation. can be changed altering activity enzymes that further modify Azacytidine prodrugs are incorporated into recognized by block function resulting hypomethylation DNA. EBV-associated cancers have genomes many carcinomas also highly cellular genomes. Decitabine, member azacytidine prodrug family, reactivates promotes recognition lymphoma cells virus-specific cytotoxic T-cells. For cancers, decitabine prospect combining other therapeutic approaches currently unknown but exciting.