Abstract
Abstract Epstein-Barr Virus (EBV) is a gamma herpesvirus that is prevalent worldwide and is an important cause of acute and chronic disease. Primary EBV infection which occurs after early childhood often results in acute infectious mononucleosis. Persistent latent EBV infection is a causative agent of anaplastic nasopharyngeal carcinoma, AIDS related lymphoma, posttransplant lymphoma, and Hodgkin's disease. Expression of Latent Membrane Protein 1 (LMP1) is common to most EBV related malignancies. LMP1 induced NF-κB activity is required for efficient transformation and survival of primary human B lymphocytes into lymphoblastoid cell lines. Increasing evidence suggest that LMP1 has an important role in the lytic cycle. Studies indicate that LMP1 and other latent genes are induced as part of the EBV lytic cascade in Burkitt's lymphomas. Our recent research indicates that LMP1-deleted virus replicates as efficiently as wildtype virus in HEK293 cells which suggests that the role of LMP1 during lytic replication is linked to changes in the cellular environment. LMP1 expression is associated with survival signals and alters expression of several differentiation markers, therefore a role for LMP1 during lytic replication in differentiating epithelial cells should be pursued. We have developed an organotypic raft culture system that will permit investigation of EBV replication in differentiating epithelial cells. Our lab is utilizing molecular, biochemical, and genetic approaches to elucidate the role of LMP1 during EBV replication in differentiating epithelial cells. We are investigating the function of LMP1 in viral replication, cell proliferation and differentiation, and viral-cellular signaling pathways. Based on these studies we will develop a model for the role of LMP1 during EBV replication in differentiating epithelial cells and its resulting pathogenesis. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 560. doi:1538-7445.AM2012-560
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