<p>Lymphomas, a significant cause of cancer morbidity worldwide, are primarily classified as Hodgkin Lymphoma (HL) or non-Hodgkin Lymphoma (NHL). The most prevalent are B-cell lymphomas, such as Diffuse Large B-Cell Lymphoma (DLBCL). A well-established body of research links a range of infections to developing these cancers. Researchers summarized current knowledge on the role of viral (e.g., Epstein-Barr virus, human immunodeficiency virus, hepatitis viruses), bacterial (e.g., <i>Helicobacter pylori</i>, <i>Chlamydia psittaci</i>), and fungal pathogens in lymphomagenesis. Fungal infections, while not direct causes of lymphoma, pose a significant threat to immunosuppressed patients. Additionally, immunodeficiency may exacerbate the development of virus-associated lymphomas, which can occur as a result of both acute infections and chronic immunological activation. The need for targeted treatments guided by their molecular pathways is underscored by the fact that these cancers are often more aggressive and resistant to therapy than solid tumors. From immediate production of viral oncoproteins to persistent antigenic stimulation, we review the many ways in which these infections promote carcinogenesis. We also emphasize the significant clinical implications of this relationship, specifically how improving patient prognosis, reducing treatment-related side effects, and, in rare instances, leading to lymphoma regression can be achieved through the precise identification and treatment of specific infections. A detailed understanding of the infectious etiology of lymphomas is essential for advancing biological insight and clinical management.</p> Graphical abstract <p></p>