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 holoendemic1. The tumour is characterized by chromosome translocations2; usually the terminal portion of chromosome 8 containing the c-myc gene is translocated to chromosome 143, near the enhancer of the immunoglobulin heavy-chain locus4. Less frequent are translocations of chromosome 8 to the κ light-chain locus of chromosome 2 or to the λ light-chain locus of chromosome 225. In vitro, EBV induces B cells to proliferate and secrete immunoglobulin and antibody6. However, in vivo the infected B lymphocytes are under immunological control, so that abnormal proliferation is found only in immunosuppressed patients7,8. Such patients are subsequently liable to develop lymphomas7,9. 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”10. 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 common11.
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Whittle, H., Brown, J., Marsh, K. et al. T-cell control of Epstein–Barr virus-infected B cells is lost during P. falciparum malaria. Nature 312, 449–450 (1984). https://doi.org/10.1038/312449a0
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DOI: https://doi.org/10.1038/312449a0
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