ArticlePLoS pathogens2014
A multifactorial role for P. falciparum malaria in endemic Burkitt's lymphoma pathogenesis.
Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.
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Who cites it
64 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.
- Estimating the global burden of Epstein-Barr virus-related cancers.Journal of cancer research and clinical oncology · 2022Pooled it
- Burkitt lymphoma: current understanding, unmet needs, and research directions.Blood advances · 2026Review
- Malaria and cancer: common features and interactions.Trends in parasitology · 2026Review
- Article
- Mechanistic interactions between Plasmodium falciparum and Epstein-Barr virus in endemic Burkitt Lymphoma pathogenesis: a narrative review (2010-2026).Infectious agents and cancer · 2026Review
- Review
- Article
- Extracellular Vesicles From Schistosoma mansoni Adult Worms Stimulate IL-10 Release by B Cells.Parasite immunology · 2025Article
- Epstein-Barr virus-infected tonsillar marginal zone B cellsJournal of virology · 2025Article
- Epstein-Barr virus type 2 infection is associated with higher viral loads in pediatric tonsils from western Kenya.Microbiology spectrum · 2025Article
- Incorporation of Epstein-Barr viral variation implicates significance of Latent Membrane Protein 1 in survival prediction and prognostic subgrouping in Burkitt lymphoma.International journal of cancer · 2025Article
- Sustained activation induced cytidine deaminase (AID) expression in B cells following Plasmodium falciparum malaria infection in Kenyan children.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Plasmodium falciparum Malaria Is Associated With Increased Kaposi Sarcoma-Associated Herpesvirus (KSHV) Seropositivity and Higher KSHV Antibody Breadth and Magnitude: Results of a Case-Control Study From Rural Uganda.The Journal of infectious diseases · 2024Article
- Human leukocyte antigen-DQA1*04:01 and rs2040406 variants are associated with elevated risk of childhood Burkitt lymphoma.Communications biology · 2024Article
- Sickle cell allele HBB-rs334(T) is associated with decreased risk of childhood Burkitt lymphoma in East Africa.American journal of hematology · 2024Article
- PfEMP1 and var genes - Still of key importance in Plasmodium falciparum malaria pathogenesis and immunity.Advances in parasitology · 2024Review
- Review
- Epstein-Barr virus infection: the micro and macro worlds.Virology journal · 2023Review
- Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2023Article
- Comparison of Epstein-Barr virus and Kaposi's sarcoma-associated herpesvirus viral load in peripheral blood mononuclear cells and oral fluids of HIV-negative individuals aged 3-89 years from Uganda.Infectious agents and cancer · 2023Article
4 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 5 institutions in 2 countries.
Funding
Abstract
Endemic Burkitt's lymphoma (eBL) arises from the germinal center (GC). It is a common tumor of young children in tropical Africa and its occurrence is closely linked geographically with the incidence of P. falciparum malaria. This association was noted more than 50 years ago. Since then we have learned that eBL contains the oncogenic herpes virus Epstein-Barr virus (EBV) and a defining translocation that activates the c-myc oncogene. However the link to malaria has never been explained. Here we provide evidence for a mechanism arising in the GC to explain this association. Accumulated evidence suggests that eBL arises in the GC when deregulated expression of AID (Activation-induced cytidine deaminase) causes a c-myc translocation in a cell latently infected with Epstein-Barr virus (EBV). Here we show that P. falciparum targets GC B cells via multiple pathways to increase the risk of eBL. 1. It causes deregulated expression of AID, thereby increasing the risk of a c-myc translocation. 2. It increases the number of B cells transiting the GC. 3. It dramatically increases the frequency of these cells that are infected with EBV and therefore protected from c-myc induced apoptosis. We propose that these activities combine synergistically to dramatically increase the incidence of eBL in individuals infected with malaria.
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