Approximately 15-20% of global cancer incidence is causally linked to viral infection. Although a number of these viruses are implicated in the aetiology of lymphomas or leukaemias, the vast majority are associated with malignancies of epithelial cells. In epithelial tissues, several classes of proteins are involved in maintaining tissue architecture, including those that promote cell-cell adhesion and others which mediate cell-matrix interactions. Previous studies have shown that the EBV-encoded oncogene, latent membrane protein-l (LMPl), altered the morphology of SCC12F cells in vitro, downregulated cell-cell adhesion molecules and promoted cell motility. To understand better the mechanism(s) by which LMPI induces these effects, transcriptional profiling was performed on SCC12F cells expressing LMPI under the control of a tetracycline-regulatable promoter. Of the many sets of genes whose expression was differentially regulated by LMPl, a large number were found to be characteristically over-expressed in inflammatory and hyperproliferative epidermal disorders such as psoriasis. These included cytokines and their receptors, growth factors involved in promoting cutaneous wound healing and cellular proliferation, and signalling molecules that regulate cell motility. Among the genes whose expression was significantly induced by LMP1 were activin A, a key orchestrator in the keratinocyte wound response, and interleukin-l, which is involved in modulating activin A. Findings presented in this thesis suggest that alterations in the interleukin-l signalling network may be responsible for many of the changes in host cell gene expression induced in response to LMPI. This helps to define the mechanism(s) by which this viral oncoprotein may influence cellular pathways regulating the balance between proliferation and differentiation, cell motility and inflammation, which are so often deregulated in wounded keratinocytes.