Abstract Malaria still kills up to 500,000 people annually. Risk factors contributing to severe disease remain poorly understood. There is compelling evidence that acute gammaherpesvirus such as Epstein-Barr Virus (EBV) coinfections are responsible for suppressing the development of humoral immunity during Plasmodium infection in children and may constitute a salient risk factor for disease severity. However, the actual mechanisms by which protective humoral immune responses to Plasmodium infection are suppressed by gammaherpesviruses are incompletely understood. It has previously been shown that acute MHV68 co-infection resulted in the transformation of a non-lethal Plasmodium yoelii XNL infection into a lethal one in C57BL/6 mice, an outcome linked to a defect in the maintenance of germinal center B cells and T follicular helper cells (Tfh) cells in the spleen and a defect in antibody production. Since the suppressive effect requires the M2 latency associated protein of MHV68, and M2 induces IL-10 secretion from the B cells it infects, we tested the hypothesis that the induction of IL-10 by M2 in MHV68-infected B cells impairs the ability of T follicular helper cells (Tfh) to provide B cell help for effective, broad spectrum antibody production to incoming Plasmodium infection. We tested our hypothesis by co-infecting mice that cannot produce IL-10 from B cells (IL-10Flox_CD19 Cre+), and measured the effect that this defect has on Tfh maintenance, plasma cell formation and antibody production in response to Plasmodium infection. Our findings suggest B cell derived IL-10 is an important component of MHV68-mediated disruption in germinal center formation during gammaherpesvirus/ Plasmodium co-infections.