Abstract
Acute Plasmodium falciparum malaria in African children allows expansion of latent Epstein-Barr virus infection, leading to colonization of lymph nodes by virus-infected lymphoblasts in 60% of cases as demonstrated by in situ hybridization for the detection of EBER-1 and EBER-2 RNA. This probably arises against a background of malaria-induced immunosuppression to EBV and concurrent lymphoid activation. The relevance of the results to the pathogenesis of African endemic Burkitt's lymphoma is discussed.
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