A recent study published has revealed the molecular link between malaria infection and Burkitt lymphoma (BL)—the most common childhood cancer in equatorial Africa and New Guinea (Figure 1). The research identifies Plasmodium falciparum, the deadliest malaria parasite, as a direct contributor to the cancer’s development by activating a gene-altering enzyme in B cells.
Figure 1: Comparison of AID expression levels in children with uncomplicated malaria and community controls, eBL and TMC from Kisumu and US. (A) Frequency of CD19+AID+ cells in children with uncomplicated malaria, recovery, and community controls. (B) Frequency of CD19+AID+ cells in children with uncomplicated malaria, eBL, and community controls. (C) Frequency of CD19+AID+ cells in tonsils from children with differential malaria exposure, ie Kisumu vs. US. (D) Geometric-MFI (G-MFI) in children with uncomplicated P. falciparum malaria during the clinical disease, recovery, and community controls; (E) G-MFI AID levels in children with uncomplicated malaria, eBL, and community controls. (F) G-MFI AID levels in tonsils from children from Kisumu (Kenya) and US. Centerlines represent medians, with lower and upper boundaries of the boxes representing the first and third quartiles, respectively. Mann–Whitney U test was performed on the different groups, and *P value <0.05 was considered significant. ****P < 0.00001, ***P < 0.0001, **P < 0.001, *P < 0.01. Acute: uncomplicated disease; 4wks: recovery at 4 weeks; 8wks: recovery at 8 weeks.
Key Discoveries
- Burkitt Lymphoma (BL) is a B-cell cancer marked by MYC gene translocation, a genetic event that drives uncontrolled cell growth.
- Malaria and Cancer Link – this is the first study to pinpoint the biological mechanism behind this link.
Researchers found elevated levels of AID (activation-induced cytidine deaminase) in the B cells of children with uncomplicated P. falciparum malaria.
- AID is the enzyme responsible for causing MYC gene translocation, the defining mutation in Burkitt lymphoma.
- Functional tests confirmed that the AID produced during malaria was fully active, strongly supporting its role in initiating cancerous mutations.
- Participants: Children diagnosed with uncomplicated malaria (non-severe symptoms) were compared with malaria-free controls.
- Children with malaria showed significantly higher AID expression in B cells, suggesting an environment primed for oncogenic transformation.
Public Health Implications
- BL is 10 times more prevalent in regions with persistent P. falciparum transmission.
- By targeting malaria through public health interventions, such as improved prevention, early treatment, and vaccine deployment, it may be possible to reduce the incidence of this deadly childhood cancer.
This study closes a long-standing gap in understanding how a parasitic infection can spark cancer by demonstrating a direct molecular link between malaria and oncogenic risk in B cells. The findings emphasise that fighting malaria may save lives not only by preventing infection but also by preventing cancer.
Journal article: Ariera, B., et al., 2025. Sustained activation induced cytidine deaminase (AID) expression in B cells following Plasmodium falciparum malaria infection in Kenyan children. The Journal of Immunology.
Summary by Stefan Botha
