Expression data from CCL185 carcinoma cell line transiently infected with EBV
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE37048 | GEO | 2012/04/11
SECONDARY ACCESSION(S): PRJNA157827
REPOSITORIES: GEO
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Project description: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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Project description:Approximately 90% of the world population is infected with EBV and carries the virus in a silent, asymptomatic state for life. In immunocompromised individuals, EBV infection can cause B-cell transformation and malignancies. One approach to control EBV infectivity is by changing the expression of viral genes. We are interested in how epigenetics contributes to regulating the gene expression patterns adopted by EBV during latency. The host’s hijacking is a well know strategy adopted by viruses to modify the epigenome, the trascriptome and the proteome of the host with the aim to survive and remain silent in the host. We observed that in B cells, EBV infection mimics antigen-mediated activation, resulting in the induction of specific proteins named Lamin A/C. Lamins have multiple and central roles they: provide nuclear physical support; anchor the heterochromatin to the nuclear periphery and seem to play a role in several nuclear functions requing the chromatin structure rearrangement. The interaction with lamins has already been study in the context of EBV lytic reactivation, but their role in the control of the EBV latency states and as epigenetic regulators of different EBV genes expression profiles as not been investigated. The binding of the Lamin AC to important regulatory regions of EBV genome was assessed through ChIP-Seq and, and gene expression (RNA-Seq) profiles, were evaluated in wild type and Lamin AC KO cell lines. Differences in protein and RNA expressions in B cells activated by using both EBV and a simulation of the immune response were analyzed. Our data suggest two main conclusion: lamins might contribute to the epigenetic control of EBV genes expression during latency changing the interaction of the host structural proteins with key regulatory regions in the viral genome and a possible mechanism with who EBV modifies the nucleus and hijacks cellular mechanisms.
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