| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2473258 | Current Opinion in Virology | 2015 | 7 Pages |
•EBV is an oncogenic gammaherpesvirus that transforms human primary B-cells.•EBV encoded transcription factors assemble at primed enhancers to activate cell promoters.•Phosphorylation and degradation of p21 mediated by the Pim-1 kinase is enhanced by EBNA3C.•Growth and survival of infected B cells by latent membrane protein 1 is induced by LUBAC and TRAF1.•Latent membrane protein 2 regulates the autophagosome to block death of infected cells.
EBV drives resting B cells to continuous proliferating latently infected cells. A restricted program of viral transcription contributes to latency and cell proliferation important for growth transformation. Recent interest in latency and transformation has provided new data about the roles of the EBV encoded latent proteins and non-coding RNAs. We broadly describe the transcription, epigenetic, signaling and super-enhancer functions of the latent nuclear antigens in regulating cellular transcription; the role of LMP2 in utilization of the autophagosome to control cell death, and the association between LMP1, the linear ubiquitin chain assembly complex and TRAF1 which are important for transformation. This review explores recent discoveries with new insights into therapeutic avenues for EBV related malignancies.
