Abstract
HIV-1-infected individuals are at greatly increased risk of Burkitt’s and other high- grade non-Hodgkin’s lymphomas, which arise as a late complication in the setting of advanced immunodeficiency [1]. Heterogeneous acquired lesions are present in varying subsets of these B-cell tumors, including activation of the c-myc (especially in Burkitt’s lymphoma), bcl-6, and ras protooncogenes, inactivation of the p53 tumor suppressor gene, and latent infection with the Epstein-Barr virus (EBV) [2,3]. The mechanisms by which immune dysregulation leads to B-cell lymphoma are poorly understood, but may be related to disruption of cytokine control and chronic B-cell hyperactivation. Lymphomagenesis may be a multistage process progressing from polyclonal B-cell proliferation to oligoclonal expansion of antigen-selected clones to subsequent outgrowth of a monoclonal tumor [4].
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Rabkin, C.S., Sei, S. (1999). Susceptibility Genes for AIDS and AIDS-Related Lymphoma. In: Melchers, F., Potter, M. (eds) Mechanisms of B Cell Neoplasia 1998. Current Topics in Microbiology and Immunology, vol 246. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-60162-0_14
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DOI: https://doi.org/10.1007/978-3-642-60162-0_14
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