Purpose of review: The present review summarizes the association of the different histotypes of Epstein-Barr virus (EBV)-associated lymphomas with known genetic lesions and/or oncogenic viruses. A more comprehensive understanding of the complex interplay existing between genetic abnormalities of tumor cells and the viral contribution to the development of EBV-associated lymphomas is pivotal for the development of more effective treatments.
Recent findings: Recent evidence indicates that HIV may contribute to lymphomagenesis by acting directly on B lymphocytes as a critical microenvironmental factor. The pathogenesis of EBV-associated lymphomas in patients with HIV infection is considered the result of the concerted action of different factors, mainly including impaired immune surveillance, genetic alterations, and concomitant viral infection (EBV and HIV).
Summary: Immunodeficiency states usually increase susceptibility to cancer as a result of reduced immune surveillance and enhanced chances for virus-driven oncogenesis. Lymphoma remains the most frequent neoplastic cause of death among patients infected with HIV. Several of the HIV-associated lymphomas are related to EBV infection. EBV-associated lymphomas in patients infected with HIV are heterogeneous, not only pathologically but also in terms of pathogenetic pathways and cellular derivation.