Field guide to the Epstein-Barr virus

The EBV Epigenome Researchers have published the first annotated atlas of the Epstein-Barr virus genome, creating the most comprehensive study of how the virus genome interacts with its human host during a latent infection. Epstein-Barr virus (EBV), which is thought to be responsible for one percent of all human cancers, establishes a latent infection in nearly 100 percent of infected adult humans. The atlas is designed to guide researchers toward new means of creating therapies against EBV-latent infection and the cancers associated with latent EBV infection, such as B cell lymphomas, gastric carcinomas, and nasopharyngeal carcinomas. The project provides the best look yet at how EBV interacts with the genes and proteins of its host cells.A representation of the annotated EBV “epigenome,” listing the protein and chemical decorations added to the EBV DNA that get passed along to new copies of the EBV virus. As a supplement to the EBV genome—the characterization of the virus’s genes—the atlas describes the epigenome—all the protein and chemical decorations added to the EBV DNA that get passed along to new copies of the EBV virus–and the transcriptome—the catalog of all the RNA transcripts created from EBV DNA, which are either coded into protein or serve to regulate DNA directly. The researchers discovered numerous new points of interaction between viral DNA and its host, highlighting the extensive coevolution of the virus and pointing toward possible targets for future cancer and anti-viral drugs. (Eurekalert)

 

An atlas of the epstein-barr virus transcriptome and epigenome reveals host-virus regulatory interactions. Cell Host Microbe. 16 Aug 2012, 12(2):233-245
Epstein-Barr virus (EBV), which is associated with multiple human tumors, persists as a minichromosome in the nucleus of B lymphocytes and induces malignancies through incompletely understood mechanisms. Here, we present a large-scale functional genomic analysis of EBV. Our experimentally generated nucleosome positioning maps and viral protein binding data were integrated with over 700 publicly available high-throughput sequencing data sets for human lymphoblastoid cell lines mapped to the EBV genome. We found that viral lytic genes are coexpressed with cellular cancer-associated pathways, suggesting that the lytic cycle may play an unexpected role in virus-mediated oncogenesis. Host regulators of viral oncogene expression and chromosome structure were identified and validated, revealing a role for the B cell-specific protein Pax5 in viral gene regulation and the cohesin complex in regulating higher order chromatin structure. Our findings provide a deeper understanding of latent viral persistence in oncogenesis and establish a valuable viral genomics resource for future exploration.

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