Human Immunodeficiency Virus Related Non-Hodgkin's Lymphoma
- PMID: 37275434
- PMCID: PMC10237187
- DOI: 10.2147/BLCTT.S407086
Human Immunodeficiency Virus Related Non-Hodgkin's Lymphoma
Abstract
Human immunodeficiency virus infection is related with an increased risk of hematological malignancy principally, non-Hodgkin lymphoma. Most non-Hodgkin lymphomas are acquired immunodeficiency syndrome defining and constitute greater than 50% of all acquired immunodeficiency syndrome defining cancers. The main pathogenesis mechanisms are immunodeficiency, chronic antigenic stimulation, and the ability to infect cancer cells causing direct carcinogenesis. Human immunodeficiency virus related non-Hodgkin lymphomas are heterogeneous in immunophenotyping and molecular features; and choice of drug treatments is similar with sporadic types. The main objective is to assess the epidemiology, pathogenesis, and morphology of human immunodeficiency virus related non-Hodgkin lymphoma. The searching strategy was done by searching relevant original and review articles from www.biosemanticjane/org, Google scholar, Google, and PubMed sites using keywords like; Acquired immunodeficiency syndrome, Human immunodeficiency virus, and non-Hodgkin lymphoma. In conclusion, human immunodeficiency virus infected people continue to have elevated risk of non-Hodgkin lymphoma. Diffuse large B-cell lymphomas are the most common and severe subtype. The pathogenesis of this type of lymphoma is associated with chromosomal abnormalities that deregulate the expression of various oncogenes by different viral particles and cytokines. However, the role of these viral particles and cytokines on pathogenesis is not clearly stated, so further study could be required.
Keywords: Burkitt lymphoma; acquired immunodeficiency syndrome; diffuse large B-cell lymphoma; human immunodeficiency virus; non-Hodgkin lymphoma; plasmablastic lymphoma; primary central nervous system lymphoma; primary effusion lymphoma.
© 2023 Gessese et al.
Conflict of interest statement
The authors report no conflicts of interest in this work.
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