The Epstein-Barr Virus is a human herpesvirus that is associated with African endemic Burkitt’s Lymphoma (BL) and several other cancers of lymphoid/epithelial origin. The capacity of this virus to regulate the expression of cellular adhesion molecules, such as CD44, has important implications in the pathogenesis of EBV-associated malignant disease. CD44 is a multifunctional cell surface adhesion olecule involved in cell-cell nd cell-matrix interactions. Many isoforms of CD44 exist, some of which have been mplicated in metastasis. These are generated primarily as a result of complex alternate NA splicing within the CD44 operon. In this thesis, CD44 expression was analysed in I) EBV-positive BL-cell lines and (II) EBV negative derived cell lines that express iral latent proteins either after superinfection with virus, or after stable transfection of ingle viral genes. The results obtained illustrate that the expression of EBV latent roteins correlates with the induction of standard/variant isoforms of CD44 RNA/protein in a BL cell background. When expressed as sole viral proteins, neither f the two principal viral effectors of cell transformation, the EBV latent membrane rotein 1 (LMP1) nor the EB nuclear antigen 2 (EBNA2), were sufficient to induce CD44 expression. As part of this research a novel method for detecting CD44 mRNA splice variants was developed. Labelled antisense riboprobes derived from CD44 cDNA sequences were used in Ribonuclease Protection Assays (RPA) to analyse standard/variant exon usage in a range of cell lines including EBV-infected cells. The results obtained with this assay also indicated that the pattern of CD44 standard and variant exon usage is very complex but similar in type-III latency BL cell lines and lymphoblastoid cell lines.