Abstract
The Epstein-Barr virus (EBV) double-stranded DNA genome is subject to extensive epigenetic regulation. Large consortiums and individual labs have generated a vast number of genome-wide data sets on human lymphoblastoid and other cell lines latently infected with EBV. Analysis of these data sets reveals important new information on the properties of the host and viral chromosome structure organization and epigenetic modifications. We discuss the mapping of these data sets and the subsequent insights into the chromatin structure and transcription factor binding patterns on latent EBV genomes. Colocalization of multiple histone modifications and transcription factors at regulatory loci are considered in the context of the biology and regulation of EBV.
Highlights
Epstein-Barr virus (EBV) is a human gammaherpesvirus that establishes long-term latent infection in B-lymphocytes [2,3]
While most cells maintain the viral genome in a type III latent state, a percentage of cells in the population can undergo spontaneous lytic replication, and the extent of this lytic replication depends on the lymphoblastoid cell lines (LCLs) and culture conditions [6]
Many CTCF binding sites are proximal to RNA polymerase regulatory elements, which is in contrast to the host genome, where the vast majority of CTCF sites are located at positions far from transcription initiation
Summary
Epstein-Barr virus (EBV) is a human gammaherpesvirus that establishes long-term latent infection in B-lymphocytes [2,3]. In LCLs, the majority of viral genomes adopt a gene expression program, referred to as type III latency, which represents the most permissive form of latent infection [4]. The type III latency-associated gene expression program in LCLs consists of nine protein coding genes, 21 microRNAs and several non-coding RNAs. The protein coding genes include the Epstein-Barr Nuclear Antigens (EBNAs) EBNA-LP, 1, 2, 3a, 3b and 3c, as well as the Latency Membrane Proteins, LMP1, LMP2a and LMP2b. Lytic origins of DNA replication remain mostly inactive in LCLs, but contain promoters for non-coding RNAs and miRNAs that can be generated at high levels during latency. How these genetic elements are coordinately regulated may be partly revealed through analysis of the viral epigenome
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