Malaria and Burkitt Lymphoma

Table of Contents

1. What the Presentation Said
2. What Burkitt Lymphoma Is
3. Denis Burkitt’s Map and the Discovery of a Virus
4. Epstein-Barr Virus: Necessary but Not Sufficient
5. Why Only Plasmodium falciparum?
6. How Malaria May Help the Virus: AID and MYC
7. What Studies of Children Show
8. How the International Cancer Agency Classifies Malaria
9. Bed Nets and Burkitt Lymphoma Rates
10. Treatment and Survival in Africa
11. How the Claim Compares With the Research
12. What Is Not Known
13. Connections
14. Key Research Papers
15. Featured Videos

What the Presentation Said

The presentation was a 2026 webinar on cancer and parasites given by the medical director of an integrative cancer clinic. It did not mention malaria or Burkitt lymphoma by name. This page takes up a general argument the speaker made, because the malaria–Burkitt story is the clearest test of that argument in the medical literature.

The points as made were:

• Parasites contribute to cancer through a chain of events. The speaker described infection leading to inflammation (“cancer is an inflammatory disease”), then to immune dysregulation in which the immune system cannot detect the parasites and other microbes, and then to higher tumour susceptibility. The speaker called this parasite-driven oncogenesis (the formation of cancer) and listed four mechanisms: chronic inflammation, oxidative stress, immune suppression and epigenetic change (changes in how genes are switched on and off).
• Parasites keep company with viruses and bacteria. The speaker said parasites harbour viruses, bacteria and heavy metals, called them “buddies” of viruses, and said that when viruses, mould, bacteria and parasites are all present, the parasites are to be treated first, because treating viruses first will not reach the viruses the parasites carry.
• Parasites are part of the tumour environment. The speaker said that in a cancer situation parasites are part of the tumour microenvironment, and that they suppress immune signalling so that disease can flourish.

The sections below report what the research on one parasite, one virus and one cancer shows about each of these points.

What Burkitt Lymphoma Is

Burkitt lymphoma is an aggressive form of non-Hodgkin lymphoma — a cancer of B cells, the white blood cells that make antibodies (Quintana and colleagues, 2020). Its defining feature is a MYC translocation: a piece of chromosome carrying the MYC gene, which pushes cells to grow and divide, is swapped next to an antibody (immunoglobulin) gene. Because antibody genes are very active in B cells, MYC is switched on all the time and drives the cancer cells to multiply (Magrath, 2012). Every Burkitt tumour carries this kind of translocation (Moormann and Bailey, 2016).

Three forms

Doctors have long described three forms, classified by where and in whom the cancer appears (Moormann and Bailey, 2016; O’Connor and colleagues, 2026):

• Endemic Burkitt lymphoma — found where P. falciparum malaria is heavily transmitted, mainly equatorial Africa and Papua New Guinea. It mostly affects young children, often appears in the jaw or abdomen, and contains Epstein-Barr virus in more than 90% of cases. Its incidence is about ten times higher than Burkitt lymphoma elsewhere.
• Sporadic Burkitt lymphoma — the form seen in the rest of the world, where about 30% of tumours contain the virus.
• Immunodeficiency-associated Burkitt lymphoma — seen mainly in adults with human immunodeficiency virus (HIV), where about 40% of tumours contain the virus.

Researchers now also classify Burkitt tumours by whether they contain Epstein-Barr virus, because virus-positive and virus-negative tumours differ at the molecular level, and this is starting to replace the older geographic labels (Moormann and colleagues, 2025; O’Connor and colleagues, 2026).

Denis Burkitt’s Map and the Discovery of a Virus

In 1958 Denis Burkitt, a surgeon working in Uganda, published a description of a tumour of the jaws in African children in the British Journal of Surgery (Burkitt, 1958). In 1962 he published a further paper in the British Medical Journal on the climatic limits of this children’s cancer in Africa (Burkitt, 1962). The striking overlap between where the tumour occurred and where P. falciparum malaria was common was noted shortly after the 1958 description (Quintana and colleagues, 2020). Studies in malaria-endemic regions have repeated Burkitt’s observation since, finding that the cancer’s incidence follows the intensity of malaria transmission (Moormann and Bailey, 2016; Magrath, 2012).

The geography suggested an infectious cause, possibly spread by insects. In 1964 M. A. Epstein, B. G. Achong and Y. M. Barr reported virus particles in cells grown from a Burkitt tumour (Epstein and colleagues, 1964). That virus, now called the Epstein-Barr virus, was the first virus found in a human cancer (Moormann and colleagues, 2025; Rochford and Moormann, 2015).

So the story has two infections from the start: a parasite whose map matched the cancer, and a virus found inside the cancer cells.

Epstein-Barr Virus: Necessary but Not Sufficient

Epstein-Barr virus is a herpes virus carried by more than 95% of adults worldwide. In most of these people it causes no symptoms, and it persists inside B cells for life (Münz, 2023; Chene and colleagues, 2009). It is also linked to several cancers of lymph and lining cells.

African children in malaria regions are infected very early: most have antibodies to the virus by the age of three, while in wealthier countries infection tends to come later (Chene and colleagues, 2009). After infection the virus is shed in saliva for life.

Reviews describe the virus as necessary but not sufficient for endemic Burkitt lymphoma: almost every endemic tumour contains it, but almost every child in the region carries it and only a tiny number develop the cancer. Something else has to tip the balance, and malaria is the leading candidate (Moormann and colleagues, 2011). A case-control study in Malawi (271 children with endemic Burkitt lymphoma, 171 controls) found that high antibody levels against the virus’s “lytic” proteins — the proteins made when the virus is actively copying itself — were strongly associated with the cancer (odds ratio 8.67 for the highest versus lowest third) (Aguilar and colleagues, 2017).

The International Agency for Research on Cancer (IARC), the cancer agency of the World Health Organization, lists Epstein-Barr virus in Group 1, its highest category: “carcinogenic to humans” (International Agency for Research on Cancer List of Classifications).

Why Only Plasmodium falciparum?

Several malaria parasites infect people, including P. vivax, P. ovale, P. malariae and P. knowlesi. The link with Burkitt lymphoma is specific to P. falciparum, the species behind most severe malaria in Africa. A 2020 review notes that exposure to P. falciparum appears to be essentially a prerequisite for endemic Burkitt lymphoma, while other human malaria parasites appear to have no impact, and that why this is so remains unexplained (Quintana and colleagues, 2020).

One explanation proposed is a protein on the surface of red cells infected with P. falciparum, called PfEMP1. In laboratory work, a part of this protein (the CIDR1α region) acted as a broad activator of B cells, helped them survive, and made B cells already carrying Epstein-Barr virus start producing virus again — including cells from healthy carriers and from children with Burkitt lymphoma. The authors described this as the first demonstration that another pathogen can directly reactivate the virus. These were cell experiments, not studies in children (Chene and colleagues, 2009).

How Malaria May Help the Virus: AID and MYC

Research has assembled several mechanisms, none proven to be the whole answer. Reviews describe two compatible theories and a set of molecular steps that link them (Moormann and colleagues, 2011; Moormann and Bailey, 2016; Msami, 2026).

1. More infected B cells and more active virus

Acute and chronic malaria strongly stimulate B cells, raise antibody levels in the blood and sharply increase the amount of Epstein-Barr virus circulating in the blood (Chene and colleagues, 2009). In a cross-sectional study of 169 Kenyan children aged 1 to 14, those living where malaria is transmitted all year had higher antibodies to the virus’s lytic and latent proteins at every age, while children from a lower-malaria area had lower levels that fell with age — a pattern the authors read as long-term reactivation of the virus under chronic malaria (Piriou and colleagues, 2009).

2. Weaker immune control of the virus

The second theory is that T cells that normally keep Epstein-Barr virus in check work less well during repeated malaria. Children who live with chronic malaria adapt their immune responses to limit life-threatening inflammation, and researchers propose that this “immune conditioning” also weakens surveillance of the virus (Moormann and colleagues, 2025). This matches the presentation’s point about immune dysregulation, but the mechanism runs through the child’s own immune adaptation to the parasite.

3. The AID enzyme and the MYC break

The MYC translocation needs DNA breaks. B cells make an enzyme called activation-induced cytidine deaminase (AID) that deliberately mutates and cuts antibody genes in germinal centres (the training camps inside lymph nodes where B cells improve their antibodies). AID is very likely what creates the breaks behind the MYC translocation (Magrath, 2012). Malaria-related molecules that stimulate an immune sensor called Toll-like receptor 9 switch AID on, which gives malaria a direct route to the key genetic accident (Magrath, 2012).

• In Kenyan children: children with uncomplicated malaria had more B cells containing AID than community controls, and the high level lasted up to 8 weeks after the parasites had been cleared; 52% of the AID was found inside the cell nucleus, where DNA is. In cell culture, the virus, a malaria-like DNA signal and a malaria-induced growth factor (BAFF) each switched AID on, and together raised the share of AID-positive cells by about 30% more than any one alone (Ariera and colleagues, 2025).
• In tumour DNA: both the virus and malaria also raised a related family of enzymes (APOBEC3), but when researchers looked at the mutations in endemic Burkitt tumours, the extra mutations matched only AID’s signature (Summerauer and colleagues, 2022).
• In germinal centres: a laboratory study proposed that P. falciparum acts through several routes at once — deregulated AID, more B cells passing through germinal centres, and many more of those cells infected with the virus, which protects them from the cell death a MYC translocation would normally trigger (Torgbor and colleagues, 2014).
• In mice: chronic infection with a mouse malaria parasite (Plasmodium chabaudi) caused prolonged germinal-centre expansion, widespread DNA damage in germinal-centre B cells and chromosome translocations. Infection did not change the overall rate of lymphoma in the mice, but shifted the lymphomas toward mature B-cell types that depended on AID and carried translocations (Robbiani and colleagues, 2015). This was done without Epstein-Barr virus, which does not infect mice.

A less tested idea

One author has proposed that the malaria parasite concentrates vitamin A and that repeated malaria exposes tissues to toxic retinoid levels that activate the virus and AID (Mawson and Majumdar, 2017). This is a hypothesis paper; no study testing it directly was found.

What Studies of Children Show

Although the geographic link is strong, studies that compare individual children with and without the cancer give mixed results.

• A meta-analysis found no clear link at the individual level. Pooling ten case-control studies, a 2021 systematic review found that current or past malaria infection did not raise the odds of endemic Burkitt lymphoma (odds ratio 0.87, 95% confidence interval 0.54–1.39). Raised antibodies against malaria showed a borderline association (odds ratio 1.50, 1.00–2.25, p = 0.051). The studies disagreed strongly with each other, and the authors called for long-term follow-up studies (Kotepui and Kotepui, 2021).
• The risk may follow quiet, long-term infection rather than sick episodes. Comparing 4,019 children with endemic Burkitt lymphoma with more than 80,000 children tested for malaria, plus 850 cases and 2,878 controls from a three-country East African study, researchers found the children with the cancer most resembled children with asymptomatic malaria parasites (similar age, haemoglobin and parasite density), not those with clinical malaria (Redmond and colleagues, 2020).
• Lifetime malaria exposure tracks the risk. Using detailed malaria maps for 49 districts in Kenya, Uganda and Tanzania, a 2023 study estimated a median of 47 malaria infections per child by age 10 (range 4 to 315). Endemic Burkitt lymphoma incidence rose 39% for each 100 extra lifetime infections, with risk peaking at ages 5 to 11; recent exposure alone did not predict risk (Broen and colleagues, 2023).
• Antibody patterns suggest chronic exposure. In the Malawi study, children with the cancer had slightly higher antibodies against one blood-stage malaria protein (odds ratio 1.29) and a pattern the authors read as more persistent malaria exposure and weaker short-term (immunoglobulin M (IgM)) responses (Aguilar and colleagues, 2017).
• A malaria-protective gene did not protect against the cancer. Sickle cell trait protects against severe malaria. In 306 Kenyan children with endemic Burkitt lymphoma and 537 matched controls, sickle cell trait was about equally common (23.8% versus 27.0%; odds ratio 0.85, not significant). Children in high-malaria areas did carry more virus-infected B cells than those in lower-malaria areas (Mulama and colleagues, 2014).

Put together, the research points to heavy, repeated, often symptom-free malaria over years — not any single malaria illness — as the condition linked to the cancer.

How the International Cancer Agency Classifies Malaria

In 2012 an International Agency for Research on Cancer working group evaluated malaria (Volume 104 of the International Agency for Research on Cancer Monographs, published 2014). It classified “malaria (caused by infection with Plasmodium falciparum in holoendemic areas)” as probably carcinogenic to humans (Group 2A) (Bouvard and colleagues, 2012; International Agency for Research on Cancer Working Group, 2014). Holoendemic means areas where nearly everyone is infected from early childhood.

International Agency for Research on Cancer’s Advisory Group for 2025–2029 summarised the basis: limited evidence for Burkitt lymphoma in humans, together with strong mechanistic evidence that malaria reactivates Epstein-Barr virus, the main cause of Burkitt lymphoma. It noted that the human evidence was based largely on ecological studies (comparisons of places rather than of individuals), that case-control studies continue to give mixed results, and that because the cancer is rare even in endemic areas, prospective studies following children would need to be infeasibly large. It gave a re-evaluation of malaria no priority until stronger human cancer data exist (International Agency for Research on Cancer Advisory Group report, 2025–2029).

By comparison, International Agency for Research on Cancer places Epstein-Barr virus itself in Group 1, and places three parasitic worms — Schistosoma haematobium and the liver flukes Opisthorchis viverrini and Clonorchis sinensis — in Group 1 as well (International Agency for Research on Cancer List of Classifications) (see the sibling pages linked under Connections).

Bed Nets and Burkitt Lymphoma Rates

If malaria helps cause endemic Burkitt lymphoma, controlling malaria could lower its rates — a possibility reviewers raised before data existed (Moormann and colleagues, 2011).

A 2024 systematic review and meta-analysis gathered 23 studies with 66 data points and 5,226 Burkitt lymphoma cases from 17 sub-Saharan African countries where insecticide-treated bed nets were rolled out on a large scale in the 2000s. Childhood Burkitt lymphoma rates were 44% lower (95% confidence interval 12%–64%) after bed nets were introduced than before: about 1.36 per 100,000 person-years before and 0.76 after. Each 1-percentage-point rise in bed-net use over the previous 10 years was associated with a 2% fall in incidence (Schmit and colleagues, 2024).

This is a population-level, before-and-after comparison, which cannot by itself separate the effect of bed nets from other changes over the same years, and the authors note the published data may not represent all of sub-Saharan Africa. It is still the most direct evidence that reducing exposure to the parasite goes with fewer cases of the cancer.

Treatment and Survival in Africa

Burkitt lymphoma is aggressive and fast-growing (Msami, 2026). In high-income countries it is reported to be highly curable with intensive chemotherapy (Painschab and colleagues, 2019). In Africa, results depend heavily on stage, delay to diagnosis, supportive care and whether treatment is completed. Antimalarial drugs are not a treatment for the lymphoma; the studies below are of chemotherapy.

• Cyclophosphamide alone, Malawi (1991–1997): when funding limited treatment to one drug, 40 of 73 children who could be traced were alive at a mean of 59 months. Survival was 63.5% for tumours of the head only and 33.3% for disease in the abdomen or elsewhere. The authors noted selection bias and variable dosing prevented accurate estimates (Kazembe and colleagues, 2003).
• Cyclophosphamide plus methotrexate, Burkina Faso: in a retrospective series of 58 children with jaw and face tumours, 21 of the 28 who completed all cycles reached complete remission; overall mortality was 19% (Béogo and colleagues, 2011).
• Cameroon, 934 children (2004–2015): treated with cyclophosphamide and methotrexate given into the spinal fluid. Most (71.5%) presented at stage III. One-year survival was 53.45% overall: 77.1% for stage I, 67.9% for stage II, 55.1% for stage III and 32.4% for stage IV. The median delay from first symptoms to diagnosis was 31 days (Hesseling and colleagues, 2024).
• Seven pediatric centres, intensive multidrug protocol (2009–2015): in 400 children with advanced disease, 12-month overall survival was 60%; 22% abandoned treatment and 49 deaths were related to treatment toxicity. Children with stage III disease who started the second course within 34 days had 76% survival versus 57% beyond 34 days (Bouda and colleagues, 2019).
• Adolescents and adults, Malawi (2013–2018): among 35 participants (43% with human immunodeficiency virus), 1-year overall survival was 40%; most deaths were from progressing lymphoma, and more intensive chemotherapy was associated with lower mortality (Painschab and colleagues, 2019).

Reviewers also describe work toward vaccines against Epstein-Barr virus as a possible way to prevent the virus-associated form of the cancer (Rochford and Moormann, 2015). No such vaccine has been shown to prevent Burkitt lymphoma. Decisions about cancer treatment and antiparasitic medicines belong with a clinician.

How the Claim Compares With the Research

What the research supports

• A parasite can contribute to a human cancer. International Agency for Research on Cancer classifies P. falciparum malaria in holoendemic areas as probably carcinogenic (Group 2A), and population studies tie the cancer’s rates to lifetime malaria exposure (Broen and colleagues, 2023) and to the spread of bed nets (Schmit and colleagues, 2024).
• Parasites and viruses can act together. Published studies report that malaria reactivates Epstein-Barr virus and increases virus-carrying B cells; this partnership is the leading explanation for endemic Burkitt lymphoma.
• Immune dysregulation is part of the mechanism. Research describes weaker control of the virus by T cells in children with chronic malaria, and malaria-driven switching-on of the DNA-cutting enzyme AID.

What it supports only in part

• Inflammation and DNA damage. Malaria-driven germinal-centre activity and AID-linked DNA damage fit the presentation’s inflammation and mutation points, but the specific route is an antibody-editing enzyme in B cells, shown most directly in mice (Robbiani and colleagues, 2015) and in blood and cell studies in children (Ariera and colleagues, 2025).
• “The immune system can’t detect the parasites.” In this case the issue described in research is the reverse: the child’s immune system responds to the parasite so strongly and so often that it adapts, and control of the virus weakens.
• Strength of the link. International Agency for Research on Cancer rates the human evidence as limited, and a meta-analysis of case-control studies found no clear link at the level of individual children (Kotepui and Kotepui, 2021).

What it contradicts

• “Parasites harbour the viruses.” The malaria parasite does not carry Epstein-Barr virus. The virus lives in the child’s own B cells and spreads through saliva; the parasite affects it indirectly, through the immune system. None of the studies reviewed here describe malaria parasites inside Burkitt tumours.
• Only one kind of malaria parasite matters. The research reports that the link is specific to P. falciparum and not to other human malaria parasites (Quintana and colleagues, 2020), which does not fit a general rule that parasites drive cancer.

What has no research

• “Treat the parasites first.” No clinical trial was found that tested treating malaria before chemotherapy, or treating parasites before viruses, as a way to improve Burkitt lymphoma outcomes. The documented treatment is chemotherapy. In one study, the AID changes in children’s B cells lasted up to 8 weeks after the parasites were cleared (Ariera and colleagues, 2025), and the risk follows years of cumulative exposure rather than recent infection (Broen and colleagues, 2023).

What Is Not Known

• Why P. falciparum, and not other malaria parasites, is linked to the cancer (Quintana and colleagues, 2020).
• Which of the proposed mechanisms — virus reactivation, loss of T-cell control, AID-driven DNA breaks, or more cells passing through germinal centres — matters most, or whether all are needed. Reviews describe the current models as partly inferential (Msami, 2026).
• Why case-control studies disagree with the strong geographic data. International Agency for Research on Cancer names measuring past malaria exposure in individual children as the main barrier (International Agency for Research on Cancer Advisory Group report, 2025–2029).
• How much of the fall in Burkitt lymphoma after bed-net rollout is due to less malaria rather than other changes over the same period (Schmit and colleagues, 2024).
• Whether a vaccine against Epstein-Barr virus could prevent endemic Burkitt lymphoma (Rochford and Moormann, 2015).
• Whether the variety of Epstein-Barr virus strains matters: Kenyan virus genomes showed extensive recombination, and some recombinant types were associated with the cancer (Agwati and colleagues, 2022).

Connections

• Cancer and Parasites
• Parasites Classified as Cancer-Causing Agents
• How Parasites Can Drive Cancer: The Mechanisms
• Do Parasites Harbour Bacteria and Viruses?
• How Parasites Evade the Immune System
• Malaria — The Plasmodium Parasite
• Malaria in Pregnancy and Children
• Antimalarial Drugs and Artemisinin Combination Therapy
• Non-Hodgkin Lymphoma
• Lymphoma
• Lymphoma: History and Discovery
• Mononucleosis
• Sickle Cell Disease
• Human Immunodeficiency Virus/Acquired Immunodeficiency Syndrome

Key Research Papers

1. Burkitt D. A sarcoma involving the jaws in African children. Br J Surg. 1958;46(197):218-23. PubMed PMID: 13628987
2. Burkitt D. Determining the climatic limitations of a children’s cancer common in Africa. Br Med J. 1962;2(5311):1019-23. PubMed PMID: 14017064
3. Epstein MA, Achong BG, Barr YM. Virus particles in cultured lymphoblasts from Burkitt’s lymphoma. Lancet. 1964;1(7335):702-3. PubMed PMID: 14107961
4. Moormann AM, Bailey JA, Rochford R. Burkitt Lymphoma. Curr Top Microbiol Immunol. 2025. PubMed PMID: 41128782
5. Rochford R, Moormann AM. Burkitt’s Lymphoma. Curr Top Microbiol Immunol. 2015;390(Pt 1):267-85. PubMed PMID: 26424650
6. Moormann AM, Bailey JA. Malaria - how this parasitic infection aids and abets EBV-associated Burkitt lymphomagenesis. Curr Opin Virol. 2016;20:78-84. PubMed PMID: 27689909
7. Moormann AM, Snider CJ, Chelimo K. The company malaria keeps: how co-infection with Epstein-Barr virus leads to endemic Burkitt lymphoma. Curr Opin Infect Dis. 2011;24(5):435-41. PubMed PMID: 21885920
8. Quintana MDP, Smith-Togobo C, Moormann A, Hviid L. Endemic Burkitt lymphoma - an aggressive childhood cancer linked to Plasmodium falciparum exposure, but not to exposure to other malaria parasites. APMIS. 2020;128(2):129-135. PubMed PMID: 32133709
9. Magrath I. Epidemiology: clues to the pathogenesis of Burkitt lymphoma. Br J Haematol. 2012;156(6):744-56. PubMed PMID: 22260300
10. Chene A, Donati D, Orem J, Mbidde ER, Kironde F, Wahlgren M, Bejarano MT. Endemic Burkitt’s lymphoma as a polymicrobial disease: new insights on the interaction between Plasmodium falciparum and Epstein-Barr virus. Semin Cancer Biol. 2009;19(6):411-20. PubMed PMID: 19897039
11. Piriou E, Kimmel R, Chelimo K, Middeldorp JM, Odada PS, Ploutz-Snyder R, Moormann AM, Rochford R. Serological evidence for long-term Epstein-Barr virus reactivation in children living in a holoendemic malaria region of Kenya. J Med Virol. 2009;81(6):1088-93. PubMed PMID: 19382256
12. Ariera B, Guyah B, Rahkola J, Arao I, Waomba K, Koech E, Samayoa-Reyes G, Sabourin KR, Ogolla S, Rochford R. Sustained activation induced cytidine deaminase (AID) expression in B cells following Plasmodium falciparum malaria infection in Kenyan children. J Immunol. 2025;214(5):926-935. PubMed PMID: 40085439
13. Summerauer AM, Jäggi V, Ogwang R, et al. Epstein-Barr virus and malaria upregulate AID and APOBEC3 enzymes, but only AID seems to play a major mutagenic role in Burkitt lymphoma. Eur J Immunol. 2022;52(8):1273-1284. PubMed PMID: 35503749
14. Torgbor C, Awuah P, Deitsch K, Kalantari P, Duca KA, Thorley-Lawson DA. A multifactorial role for P. falciparum malaria in endemic Burkitt’s lymphoma pathogenesis. PLoS Pathog. 2014;10(5):e1004170. PubMed PMID: 24874410
15. Robbiani DF, Deroubaix S, Feldhahn N, et al. Plasmodium Infection Promotes Genomic Instability and AID-Dependent B Cell Lymphoma. Cell. 2015;162(4):727-37. PubMed PMID: 26276629
16. Kotepui KU, Kotepui M. Malaria Infection and Risk for Endemic Burkitt Lymphoma: A Systematic Review and Meta-Analysis. Int J Environ Res Public Health. 2021;18(11):5886. PubMed PMID: 34070881
17. Redmond LS, Ogwang MD, Kerchan P, et al. Endemic Burkitt lymphoma: a complication of asymptomatic malaria in sub-Saharan Africa based on published literature and primary data from Uganda, Tanzania, and Kenya. Malar J. 2020;19(1):239. PubMed PMID: 32718346
18. Broen K, Dickens J, Trangucci R, et al. Burkitt lymphoma risk shows geographic and temporal associations with Plasmodium falciparum infections in Uganda, Tanzania, and Kenya. Proc Natl Acad Sci U S A. 2023;120(2):e2211055120. PubMed PMID: 36595676
19. Aguilar R, Casabonne D, O’Callaghan-Gordo C, et al. Assessment of the Combined Effect of Epstein-Barr Virus and Plasmodium falciparum Infections on Endemic Burkitt Lymphoma Using a Multiplex Serological Approach. Front Immunol. 2017;8:1284. PubMed PMID: 29123514
20. Mulama DH, Bailey JA, Foley J, et al. Sickle cell trait is not associated with endemic Burkitt lymphoma: an ethnicity and malaria endemicity-matched case-control study suggests factors controlling EBV may serve as a predictive biomarker for this pediatric cancer. Int J Cancer. 2014;134(3):645-53. PubMed PMID: 23832374
21. Schmit N, Kaur J, Aglago EK. Mosquito Bed Net Use and Burkitt Lymphoma Incidence in Sub-Saharan Africa: A Systematic Review and Meta-Analysis. JAMA Netw Open. 2024;7(4):e247351. PubMed PMID: 38635267
22. Bouvard V, Baan RA, Grosse Y, et al.; WHO International Agency for Research on Cancer Monograph Working Group. Carcinogenicity of malaria and of some polyomaviruses. Lancet Oncol. 2012;13(4):339-40. PubMed PMID: 22577663
23. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Malaria and some polyomaviruses (SV40, BK, JC, and Merkel cell viruses). IARC Monogr Eval Carcinog Risks Hum. 2014;104:9-350. PubMed PMID: 26173303
24. Münz C. Modulation of Epstein-Barr-Virus (EBV)-Associated Cancers by Co-Infections. Cancers (Basel). 2023;15(24):5739. PubMed PMID: 38136285
25. Msami NA. Mechanistic interactions between Plasmodium falciparum and Epstein-Barr virus in endemic Burkitt Lymphoma pathogenesis: a narrative review (2010-2026). Infect Agent Cancer. 2026;21(1):66. PubMed PMID: 42458528
26. Mawson AR, Majumdar S. Malaria, Epstein-Barr virus infection and the pathogenesis of Burkitt’s lymphoma. Int J Cancer. 2017;141(9):1849-1855. PubMed PMID: 28707393
27. Agwati EO, Oduor CI, Ayieko C, Ong’echa JM, Moormann AM, Bailey JA. Profiling genome-wide recombination in Epstein Barr virus reveals type-specific patterns and associations with endemic-Burkitt lymphoma. Virol J. 2022;19(1):208. PubMed PMID: 36482473
28. O’Connor E, Scanlan P, Smith OP, Halasz M. Clinical and molecular variations in Burkitt lymphoma. Transl Oncol. 2026;63:102611. PubMed PMID: 41297313
29. Kazembe P, Hesseling PB, Griffin BE, Lampert I, Wessels G. Long term survival of children with Burkitt lymphoma in Malawi after cyclophosphamide monotherapy. Med Pediatr Oncol. 2003;40(1):23-5. PubMed PMID: 12426682
30. Béogo R, Nacro B, Ouédraogo D, Ouoba K. Endemic Burkitt lymphoma of maxillofacial region: results of induction treatment with cyclophosphamide plus methotrexate in West Africa. Pediatr Blood Cancer. 2011;56(7):1068-70. PubMed PMID: 21344617
31. Hesseling PB, Afungchwi GM, Njodzeka BW, Wharin P, Kouya FN, Kruger M. Burkitt lymphoma: The effect of age, sex and delay to diagnosis on treatment completion and outcome of treatment in 934 Patients in Cameroon. PLoS One. 2024;19(3):e0299777. PubMed PMID: 38466670
32. Bouda GC, Traoré F, Couitchere L, et al. Advanced Burkitt Lymphoma in Sub-Saharan Africa Pediatric Units: Results of the Third Prospective Multicenter Study of the Groupe Franco-Africain d’Oncologie Pédiatrique. J Glob Oncol. 2019;5:1-9. PubMed PMID: 31794283
33. Painschab MS, Westmoreland KD, Kasonkanji E, et al. Prospective study of Burkitt lymphoma treatment in adolescents and adults in Malawi. Blood Adv. 2019;3(4):612-620. PubMed PMID: 30796065

PubMed Topic Searches

1. Endemic Burkitt lymphoma and Plasmodium falciparum
2. Malaria and Epstein-Barr virus reactivation in children
3. AID enzyme, malaria and Burkitt lymphoma
4. Burkitt lymphoma treatment and survival in sub-Saharan Africa

Other Sources

1. International Agency for Research on Cancer. List of Classifications, Volumes 1–123 (Epstein-Barr virus, Group 1; malaria caused by infection with Plasmodium falciparum in holoendemic areas, Group 2A). monographs.iarc.who.int
2. International Agency for Research on Cancer. Report of the Advisory Group to Recommend Priorities for the IARC Monographs during 2025–2029 (entry 016, Malaria). monographs.iarc.who.int

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