Viral participation in cellular and microenvironmental transformation and amplification towards malignancy in AIDS patients.

HIV-1 infection would initially predispose to neoplastic transformation in terms of a progressive lymphocytic proliferation followed by the onset of an immunodeficiency state. Both virion genomic integration and also active host cell proliferation would perhaps participate in the establishment of an often multifocal primary CNS lymphoma of AIDS type. Repeated opportunistic infections in AIDS patients tend to especially involve the central nervous system to also carry an increased risk of neoplastic transformation of the reactive B lymphocytes reaching the brain. A microenvironmental set of circumstances in patients with AIDS would predispose to non-Hodgkin's lymphoma largely in terms of an HIV-1 infection that progresses concurrently with evolving cell replication, immunodeficiency, and repeated opportunistic infections as caused by several different potential pathogens. Epstein-Barr virus infection in particular appears closely related to Hodgkin's disease that develops in some AIDS patients. A viral role in the development of lymphomas and of Kaposi sarcoma in HIV-infected individuals would account for neoplastic aggressiveness and for a particular predilection for primary CNS lymphoma. Such a role perhaps implicates viral integration within the genome of host cells that are actively proliferating or else infected by multiple viral pathogens such as EBV, HIV-1, CMV, and Herpes virus.