User:Blazer2023/Epstein–Barr virus

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Latency

"During latency, several copies of the viral genome are maintained as minichromosomes in the nucleus. In latently infected cells, most viral genes are epigenetically repressed by cellular chromatin constituents and DNA methylation, but certain EBV genes are spared and remain expressed to support the latent state of the virus in its host cell."

Epigenetic changes such as DNA methylation and cellular chromatin constituents, suppress the majority of the viral genes in latently infected cells. The genes that are expressed support the latent state of the virus.

Reactivation

"Reactivation is a coordinated process that requires the removal of repressive chromatin components and a gain in accessibility for viral and cellular factors and machines to support the entire transcriptional program of EBV’s ensuing lytic phase." A main trigger for reactivation of the EBV is the BZLF1 transcriptional activation domain that determines whether EBV is latent or lytic. This transcriptional activator is structurally similar to a family of transcriptional activators known as b-Zip that efficiently enhances viral E genes by binding upstream of a viral gene in the CpG methylated regions. The BZLF1 preferentially binds to CpG methylated ZRE's which is the cause for efficient downstream initiation of viral genes. There are modifications that are done to the histones in the promoter region that help to regulate BZFL1. Epigenetic factors like acetylation and phosphorylation are associated with the virus's reactivation.

Transformation of B-lymphocytes

"EBV uses the host epigenetic machinery to regulate its distinct viral gene expression states. However, epigenetic manipulation by EBV affects the host epigenome by reprogramming cells in ways that leave long-lasting, oncogenic phenotypes. Such virally-induced epigenetic alterations are evident in EBV-associated cancers."

* Possible edits to "Transformation of B-lymphocytes": The manipulation of the human body's epigenetics by EBV can alter the genome of the cell to leave oncogenic phenotypes.2 As a result the modification by the EBV increases the hosts likelihood of developing EBV related cancer.2 EBV related cancers are unique in that they are frequent to making epigenetic changes but are less likely to mutate.2