Figure 1.

Coinfections modify EBV-associated lymphomagenesis. (A) Holoendemic Plasmodium falciparum (P. falciparum) exposure is associated with endemic Burkitt’s lymphoma. The characteristic c-myc translocation in these uniformly EBV-infected tumor cells might be driven by parasite-induced B cell differentiation. (B) Primary effusion lymphoma is to 100% KSHV and to 90% EBV infected. KSHV infection drives the characteristic plasmablastic differentiation of these tumor cells that in turn leads to increased early lytic EBV reactivation. (C) HIV is able to infect EBV-transformed B cells by virtue of their CD4 upregulation and maintained CXCR4 expression. The resulting double-infected B cells with integrated HIV provirus upregulate MHC class I antigen presentation and are therefore efficiently eliminated by CD8⁺ T cells.