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Simple Summary: Epstein–Barr virus is a highly prevalent virus associated with a multitude of diseases, including autoimmune conditions such as multiple sclerosis and many types of cancer. As such, it is imperative to have a foundational understanding of this virus. This review discusses the contribution of the Epstein–Barr virus to key hematologic malignancies with a focus on the roles of latent proteins, including diffuse large B-cell lymphoma, Hodgkin lymphoma, Burkitt lymphoma, NK/T-cell lymphoma, and primary CNS lymphoma. It then provides a brief overview of treatment for each of these diseases. The clinical significance of Epstein–Barr virus (EBV) cannot be understated. Not only does it infect approximately 90% of the world's population, but it is also associated with numerous pathologies. Diseases linked to this virus include hematologic malignancies such as diffuse large B-cell lymphoma, Hodgkin lymphoma, Burkitt lymphoma, primary CNS lymphoma, and NK/T-cell lymphoma, epithelial malignancies such as nasopharyngeal carcinoma and gastric cancer, autoimmune diseases such as multiple sclerosis, Graves' disease, and lupus. While treatment for these disease states is ever evolving, much work remains to more fully elucidate the relationship between EBV, its associated disease states, and their treatments. This paper begins with an overview of EBV latency and latency-associated proteins. It will then review EBV's contributions to select hematologic malignancies with a focus on the contribution of latent proteins as well as their associated management. [ABSTRACT FROM AUTHOR]

B-cell lymphomas arise at distinct stages of cellular development andmaturation, potentially influencing antigen (Ag) presentation and T-cell recognition. Burkitt lymphoma (BL) is a highly malignant B-cell tumor associated with Epstein-Barr Virus (EBV) infection. Although BL can be effectively treated in adults and children, leading to high survival rates, its ability to mask itself from the immune system makes BL an intriguing disease to study. In this paper, we will provide an overview of BL and its association with EBV and the c-myc oncogene. The contributions of EBV and c-myc to B-cell transformation, proliferation, or attenuation of cellular network and immune recognition or evasion will be summarized. We will also discuss the various pathways by which BL escapes immune detection by inhibiting both HLA class I- and II-mediated Ag presentation to T cells. Finally, we will provide an overview of recent developments suggesting the existence of BL-associated inhibitory molecules that may block HLA class II-mediated Ag presentation to CD4+ T cells, facilitating immune escape of BL. [ABSTRACT FROM AUTHOR]