EBV is a prevalent human herpesvirus which is implicated in the aetiology of several human malignancies, including Burkitt’s Lymphoma and several other cancers of lymphoid/epithelial origin. Infection of primary B lymphocytes in vitro with EBV leads to expression of a restricted set of EBV latent genes and subsequent immortalisation of cells into continuously proliferating lymphoblastoid cell lines (LCLs). Eleven viral genes are expressed in latently-infected (immortalised) B cells, of which just six are critical for transformation. These include latent membrane protein 1 (LMP1) and five nuclear antigens (EBNA1, -2, -3A, -3C and -LP ). The first part of this study was undertaken in order to investigate the mechanism of EBV-mediated deregulation of cell growth by examining its effects on the mRNA levels of a range of cell cycle inhibitor genes using ribonuclease protection assay (Chapter 3). Significantly elevated p21 mRNA levels was found to be a characteristic feature of the transition from EBV latency type I infection (expressing EBNA1 only) to type III infection (expressing all 11 latent EBV genes) of Burkitt Lymphoma (BL) cells, with elevated expression detected in EBV-immortalised lymphoblastoid cell lines, consistent with previous reports. Western blot analysis confirmed a similar degree of upregulation at the protein level. p21 (WAF1/CIP1) is an important nuclear protein with cyclin-dependent kinase (cdk) inhibitory activity, which can promote cytostasis by blocking cell cycle progression at the Gi and/or G2 phases of the cell cycle and by inhibiting PCNA-dependent DNA replication. As EBNA2 and LMP1 are both central to the immortalisation process, the contributions of each of these proteins to the observed p21 upregulation was investigated using a tetracyclineregulatable gene expression system in an EBV-negative BL background. This revealed an important role for LMP1, but not for EBNA2 when expressed singly. LMP1 is defined as a classical oncogene and its profound effects on cell growth are well-documented. The observed LMP1-mediated upregulation of p21 was found to be a B cell-specific effect, and was not detected in a second BL-derived cell line which lacks the characteristic c-myc translocation. In addition, the effect is likely to be p53-independent. On further investigation into the mechanism of upregulation, no transactivation of the p21 promoter was detected while enhanced p21 mRNA stability was found to be important in the LMP1-mediated effect. Further studies will be required to characterise the molecular basis of this stabilisation. The precise functions of the EBNA3 proteins are unclear, although persistent expression of these genes against negative selective pressure by cytotoxic T lymphocytes in vivo is consistent with important roles for all three members of this protein family. In attempting to identify potential protein binding partners for EBNA3B, the yeast two hybrid system (YTHS) was employed to screen two cDNA libraries. Both libraries yielded only false positives, including two EBNA3B-specific interactions. However, this type of result is well-documented as a recurring problem associated with use of YTH systems.