Epstein-Barr virus (EBV) is implicated as a cause of B cell lymphoproliferative disorders in normal and immunocompromised patients and as a cause of nasopharyngeal cancer. The ability of EBV to immortalize B cells, enabling them to proliferate indefinitely in vitro, is probably a significant manifestation of its oncogenic capacity. While the principle EBV genes transcribed in latently infected cells have been identified, little is known regarding the cellular processes affected by EBV encoded products. EBV is likely to effect cell proliferation through highly specific changes in cell gene expression and by less specific induction of processes integral to cell proliferation. Using the technique of subtractive cDNA hydridization, mRNAs which are differentially expressed between EBV infected and uninfected cell lines (or between cells expressing single EBV genes and control cells converted with vector only) will be identified. The specific goals of this endeavor will be to identify potential growth regulatory functions whose expression is modulated either directly or indirectly by EBV encoded products. Together with studies of the intracellular biochemistry and physiology of EBV genes, elucidation of the cell genes whose expression is specifically or less specifically altered by EBV infection should provide important insight into the pathways by which EBV gene products induce cell proliferation.
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