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T-cell control of Epstein-Barr virus-infected B cells is lost during P. falciparum malaria
Insights
Malaria infection alters T-cells, leading to abnormal B-lymphocyte proliferation. This Epstein-Barr virus-driven process may explain increased Burkitt's lymphoma incidence in malaria-endemic regions.
Area of Science:
- Oncology
- Immunology
- Infectious Diseases
Background:
- Endemic Burkitt's lymphoma (a childhood cancer) is linked to Epstein-Barr virus (EBV) and malaria in Africa.
- This cancer involves specific chromosome translocations, often affecting the c-myc gene and immunoglobulin loci.
- Normally, EBV-infected B lymphocytes are controlled by the immune system, with abnormal proliferation occurring in immunosuppressed individuals.
Purpose of the Study:
- To investigate the immunological changes during Plasmodium falciparum malaria attacks.
- To understand how these changes might contribute to the development of Burkitt's lymphoma.
Main Methods:
- Analysis of T-cell subpopulations during Plasmodium falciparum malaria attacks.
- In vitro assessment of Epstein-Barr virus (EBV)-infected B lymphocyte proliferation and immunoglobulin secretion.
Main Results:
- Plasmodium falciparum malaria significantly alters T-cell subpopulations.
- These alterations lead to abnormal in vitro proliferation of EBV-infected B lymphocytes.
- Elevated immunoglobulin and antibody secretion by B lymphocytes was observed.
Conclusions:
- The immune dysregulation caused by P. falciparum malaria may promote abnormal B-lymphocyte proliferation.
- This phenomenon provides a potential explanation for the higher incidence of Burkitt's lymphoma in malaria-prone areas.
- The findings support the hypothesis of a link between chronic parasitic infections and lymphomagenesis.
Abstract:
Endemic Burkitt's lymphoma, a tumour of children in which B lymphocytes are infected with Epstein-Barr virus (EBV), is common in areas of Africa where malaria is holoendemic. The tumour is characterized by chromosome translocations; usually the terminal portion of chromosome 8 containing the c-myc gene is translocated to chromosome 14, near the enhancer of the immunoglobulin heavy-chain locus. Less frequent are translocations of chromosome 8 to the kappa light-chain locus of chromosome 2 or to the lambda light-chain locus of chromosome 22. In vitro, EBV induces B cells to proliferate and secrete immunoglobulin and antibody. However, in vivo the infected B lymphocytes are under immunological control, so that abnormal proliferation is found only in immunosuppressed patients. Such patients are subsequently liable to develop lymphomas. Burkitt believed that the tumour he had described resulted from interaction between a virus(es) and a "reticuloendothelial system altered by chronic and heavy infection by malarial or other parasites". We report here that during an attack of Plasmodium falciparum malaria, T-cell subpopulations are radically altered so that, in vitro, B lymphocytes infected with EBV proliferate abnormally to secrete large amounts of immunoglobulin and antibody. This phenomenon offers some explanation for the increased incidence of Burkitt's tumour and the high levels of immunoglobulin found in people living in areas where P. falciparum malaria is common.