How <i>P</i>. <i>falciparum</i> increases the risk of endemic Burkitt’s lymphoma.

<p>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) [<a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1005331#ppat.1005331.ref014" target="_blank">14</a>]. Malaria is immunosuppressive (B) [<a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1005331#ppat.1005331.ref016" target="_blank">16</a>,<a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1005331#ppat.1005331.ref017" target="_blank">17</a>], 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 <i>P</i>. <i>falciparum</i> 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 <i>P</i>. <i>falciparum</i> 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.</p