Study of the interactions between viral and human genomes during transformation of B cells with Epstein-Barr virus

Epstein-Barr virus (EBV) is a common herpes virus that establishes a life long persistence in the human host and can directly transform B lymphocytes. EBV can drive B cell development and survival in the absence of normal B cell receptor signals. The goal of our work was to define the mechanisms by which EBV regulates B cell fate. We developed new sections of TRRD and GeneNet databases containing the information on the processes occurring during EBV infection and transformation of B cells as well as about signal transduction pathways, regulatory proteins, and genes whose expression changes in transformed B cells. Analysis of the information from these new sections revealed several transcription factors important for regulation of B cell fate by EBV. The samples of corresponding binding sites were constructed, and the methods for recognizing binding sites of these factors were developed. Regulatory regions of genes expressed in B cells and the complete genome of EBV were scanned by these methods. In addition to CD23, already known from the literature data, seven most probable target genes for the viral transcription factor EBNA-2 were discovered. According to the study performed, the cellular transcription factors AP1, BSAP, NF-kappa B, STAT, and c-Myc may activate EBV promoters.