Abstract
Epstein-Barr virus (EBV) is present in Burkitt's lymphoma (BL) cells in a latent form, showing a highly restricted pattern of gene expression with few tumor cells undergoing viral lytic replication. BL cell lines can be induced to enter the viral lytic cycle and initiate replication by stimulating surface immunoglobulin molecules. During this process many EBV genes are expressed that have the potential to influence host gene expression. We aimed to identify host genes that are regulated by EBV in BL cells and those that are regulated following ligation of surface IgG. The differentially expressed genes in EBV-positive Akata cells and EBV-negative AK31 cells were detected by microarray. A total of 91 human genes were differentially expressed between Akata and AK31 cells and 198 were differentially expressed when cells were stimulated to enter lytic replication. The differential expression of one gene, myd88, was correlated with disrupted TLR9 signaling. EBV down-regulates most of the genes regulated by surface Ig cross-linking in the early stages of lytic cycle activation. These include genes involved in cell survival, signal transduction, transcription control and the immune response that may mediate EBV transformation of B-lymphocytes and others such as HDAC4 that may affect virus replication.
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