The Link between Plasmodium falciparum Malaria and Endemic Burkitt’s Lymphoma—New Insight into a 50-Year-Old Enigma

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The link between Plasmodium falciparum malaria and endemic Burkitt’s lymphoma (eBL) has been an enigma for more than 50 years, since it was first observed that the occurrence of the two coincided [1,2]. So convincing was the association that it led to the prediction that eBL was caused by an infectious agent that was spread by malarial mosquitoes. The subsequent search turned up the first human oncogenic virus, Epstein-Barr virus (EBV) [3,4]. EBV is found in nearly all cases of eBL [5] and has been shown to be a potent transforming virus for human B cells [4]. eBL is believed to arise from germinal center (GC) B cells [6] and is characterized by a typical translocation of the c-myc oncogene into one of the immunoglobulin loci [7,8]. The subsequent deregulation of c-myc expression would normally lead to rapid apoptosis of the cell, but the presence of EBV is thought to rescue these cells and allow them to survive [9]. The enigma remained, however, because EBV is not spread by mosquitoes. eBL therefore represents an intriguing and unusual situation in which interactions between a protozoan parasite (P. falciparum) and a mammalian virus (EBV) combine to cause cancer. While the mechanisms linking EBV to lymphoma development are becoming better understood, the link between P. falciparum malaria and eBL has remained completely unexplained until now. Finally, we have a breakthrough in this longstanding issue from two separate studies: one through investigation of human tissues and one in a mouse model.

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