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Burkitt Lymphoma
Ann M Moormann1, Jeffrey A Bailey2, Rosemary Rochford3
1Division of Immunology and Infectious Diseases, Department of Medicine, University of Massachusetts Chan Medical School, Worcester, MA, USA. ann.moormann@umassmed.edu.
Insights
Epstein-Barr virus (EBV) and Plasmodium falciparum (Pf) malaria coinfections in children may drive Burkitt lymphoma (BL) development. Malaria-induced immune changes could weaken surveillance, promoting EBV-driven BL tumorigenesis.
Area of Science:
- Oncology
- Virology
- Immunology
- Infectious Diseases
Background:
- Burkitt lymphoma (BL) is a significant pediatric cancer in sub-Saharan Africa.
- Epstein-Barr virus (EBV) is linked to BL, with a new classification distinguishing EBV-positive and negative tumors.
- High incidence of EBV-positive BL correlates with Plasmodium falciparum (Pf) malaria coinfections in endemic regions.
Purpose of the Study:
- To explore the link between Pf malaria coinfections and EBV-driven Burkitt lymphoma pathogenesis.
- To understand how malaria-induced immune adaptations influence EBV persistence and BL development.
Main Methods:
- Review of epidemiologic studies on EBV infections and Pf malaria.
- Analysis of immune adaptations in children from malaria holoendemic regions.
- Postulation of a mechanism involving immune conditioning, B cell proliferation, and EBV load.
Main Results:
- Pf malaria infections directly impact EBV reactivation and persistence.
- Chronic Pf malaria leads to immune adaptations to mitigate immunopathology.
- These adaptations may result in diminished EBV-specific cellular immune surveillance.
Conclusions:
- Malaria-induced immune conditioning, coupled with increased B cell proliferation and EBV load, creates a permissive environment for BL tumorigenesis.
- Understanding this interplay is crucial for developing targeted prevention and treatment strategies for pediatric BL in endemic areas.
Abstract:
Burkitt lymphoma (BL) remains a prevalent pediatric cancer in sub-Saharan Africa and was the first human cancer identified with a virus when Epstein-Barr virus (EBV) was discovered in a Ugandan BL tumor in 1964. The impact of EBV in BL is highlighted by a new molecular tumor classification of EBV positivity versus negativity which is starting to supersede longstanding epidemiologic classifications. The high incidence of EBV-positive BL in Africa and Papua New Guinea has been linked to Plasmodium falciparum (Pf) malaria coinfections in young children. Epidemiologic studies have yielded insight into early-age EBV infections and have demonstrated direct impacts of Pf malaria infections on EBV reactivation and disruptions in EBV persistence. Moreover, when children residing in malaria holoendemic regions are contending with chronic Pf malaria infections, they undergo immune adaptations to mitigate life-threatening immunopathology. We postulate that this malaria-induced immune conditioning leads to diminished EBV-specific cellular immune surveillance, when combined with higher B cell proliferation, and EBV load creates a permissive environment for BL tumorigenesis.
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