Epigenetic regulation of EBV persistence and oncogenesis.
Epigenetic mechanisms play a fundamental role in generating diverse and heritable patterns of viral and cellular gene expression. Epstein-Barr virus (EBV) can adopt a variety of gene expression programs that are necessary for long-term viral persistence and latency in multiple host-cell types and conditions. The latent viral genomes assemble into chromatin structures with different histone and DNA modifications patterns that control viral gene expression. Variations in nucleosome organization and chromatin conformations can also influence gene expression by coordinating physical interactions between different regulatory elements. The viral-encoded and host-cell factors that control these epigenetic features are beginning to be understood at the genome-wide level. These epigenetic regulators can also influence viral pathogenesis by expanding tissue tropism, evading immune detection, and driving host-cell carcinogenesis. Here, we review some of the recent findings and perspectives on how the EBV epigenome plays a central role in viral latency and viral-associated carcinogenesis.
The Fels Institute, Department of Microbiology and Immunology, Temple School of Medicine, Philadelphia, PA 19140, United States. Electronic address: Tempera@temple.edu.
Italo
I
Tempera
The Wistar Institute, Philadelphia, PA 19140, United States. Electronic address: Lieberman@wistar.org.
Paul M
PM
Lieberman
D002471:Cell Transformation, Neoplastic; D002472:Cell Transformation, Viral; D002843:Chromatin / Q000235:genetics / Q000378:metabolism; D019175:DNA Methylation; D044127:Epigenesis, Genetic; D020031:Epstein-Barr Virus Infections / Q000150:complications* / Q000821:virology; D015967:Gene Expression Regulation, Viral; D016679:Genome, Viral; D004854:Herpesvirus 4, Human / Q000502:physiology*; D006657:Histones / Q000378:metabolism; D006801:Humans; D038101:Insulator Elements; D009369:Neoplasms / Q000209:etiology*; D018741:Replication Origin; D017735:Virus Latency / Q000235:genetics
D002843:Chromatin; D006657:Histones
CTCF; Chromatin; Chromosome conformation; DNA methylation; Epstein–Barr virus; Gammaherpesvirus; Histone modifications; OriP