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How P. falciparum increases the risk of endemic Burkitt’s lymphoma.

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posted on 28.01.2016, 12:39 by David Thorley-Lawson, Kirk W. Deitsch, Karen A. Duca, Charles Torgbor

Essentially all adults are persistently infected with EBV (A). As a consequence, newly infected B cells are continually being produced that transit the GC on their way to becoming latently infected memory B cells (the site of viral persistence) [14]. Malaria is immunosuppressive (B) [16,17], and Torgbor et al. have shown that this results in a highly elevated throughput of EBV-infected cells in the GC (C). Torgbor et al. also showed that P. falciparum induces deregulated expression of the DNA-mutating and -cutting enzyme AID in GC cells (D). Robbiani et al. subsequently showed in a mouse model that this deregulated expression led to DNA damage, translocations, and, ultimately, lymphoma (E). Thus, infection with P. falciparum has been shown to have two effects on the GC, where eBL originates. Together, these increase the risk that a GC cell will undergo a c-myc translocation and that this cell will also be EBV-infected and, therefore, able to tolerate the translocation, synergistically increasing the likelihood that eBL will arise.