Lymphoma is the most common haematological malignancy in Australia of which Diffuse Large B-cell Lymphoma (DLBCL) is the most common and most aggressive form. EBV infection is a known risk factor for lymphoma development. Patients with EBV+ DLBCL have poorer outcome compared than those with EBV-ve DLBCL.  Only 30-40% of DLBCL patients respond to checkpoint inhibitors. As EBV+ DLBCL has an immune-dominant type III viral latency (with absent lytic viral expression) and antigen presentation is intact potentially rendering EBV+ tumours immunogenic, it is unknown why B-cell lymphoma (BCL) is not cleared by the immune system, but T-cell dysfunction may be responsible. Some studies suggest a generalized immune suppression may be present whereas others indicate a reduced frequency of EBV latent antigen-specific CD8+ T cells but with increased exhaustion markers expression (e.g. LAG3, PD-1 and TIM-3) suggesting antigen-specific dysfunction. Therefore it remains unclear whether BCL inactivates CD8+ T cells in an antigen-specific manner. This study aims to clarify this by comparing EBV+ and EBV-ve DLBCL and determining the frequency and phenotype of EBV lytic- and latent-specific CD8+ T cells in patients by flow cytometry. Dextramers and a panel of markers such as LAG-3, TIM-3, PD-1 and TIGIT will be used to study EBV-specific CD8+ T cells. Healthy subjects and EBV-ve DLBCL patients will be studied to establish baseline and effect of antigen-specificity on CD8+ T cells, respectively. We predict that if BCL specifically inactivates tumour-antigen specific (i.e. EBV) CD8+ T cells then latent-antigen specific but not lytic-antigen specific CD8+ T cells, will exhibit an exhausted phenotype in the setting of EBV+ tumours. The outcomes may enable identification of the mechanisms underlying the poorer prognosis for EBV+ DLBCL and provide insights into the most effective therapies for these patients.