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AIDS‐related lymphomas: from pathogenesis to pathology

Human immunodeficiency virus (HIV)‐associated lymphomas include: (1) lymphomas also occurring, although sporadically, in the absence of HIV infection. The vast majority of these lymphomas are high‐grade B‐cell lymphomas: Burkitt lymphoma (BL), diffuse large B‐cell lymphoma (DLBCL) with centroblastic (CB) features and DLBCL with immunoblastic (IBL) features; (2) unusual lymphomas occurring more specifically in HIV‐positive patients and include two rare entities, namely ‘primary effusion lymphoma’ (PEL) and ‘plasmablastic lymphoma’ of the oral cavity. The pathological heterogeneity of acquired immunodeficiency syndrome‐associated non‐Hodgkin's lymphomas (AIDS‐NHL) reflects the heterogeneity of their associated molecular lesions. In AIDS‐BL, the molecular lesions involve activation of cMYC, inactivation of P53, and infection with Epstein–Barr virus (EBV). AIDS‐IBL infected with EBV are characterised by frequent expression of latent membrane protein 1 – an EBV oncoprotein. The biological heterogeneity of AIDS‐NHL is highlighted by their histogenetic differences. Kaposi's sarcoma‐associated herpesvirus/human herpesvirus 8 (KSHV/HHV8)‐associated lymphomas, which often develop in persons with advanced AIDS, present predominantly as PEL. KSHV/HHV8 has also been recently detected in solid extracavitary‐based lymphomas. The KSHV/HHV8‐associated solid lymphomas are (1) unusual lymphomas that occur more specifically in HIV‐positive patients; (2) extracavitary and arise in nodal and/or extranodal sites; and (3) histologically, they usually display a PEL‐like morphology and plasma cell‐related phenotype.