| Description |
Malaria kills over 600,000 people a year. 67% of those deaths are children under five and pregnant women. Some children get malaria, but they do not die. The reasons for this are not completely understood. Malaria is caused by the Plasmodium parasite, and in sub-Saharan Africa Plasmodium falciparum is the main species. Co-infection of malaria with gammaherpesviruses, such as Epstein Barr Virus (EBV), is common in young children under five in countries where malaria is present. Data from children living in Cameroon in Central Africa shows that children who have EBV and malaria are more likely to be hospitalized due to malaria complications than children who do not have EBV (Joyner et al., manuscript in preparation). Antibodies are one of the main weapons the immune system uses to fight malaria. EBV suppressed anti-malarial antibody production, possibly by induction of IL-10, a molecule that prevents B cells from producing antibodies. EBV induces IL-10 production in infected cells and can synthesize a homolog of IL-10. We hypothesize that the IL-10 induced during EBV infection results in lower antibody titers in children who are infected with both the virus and Plasmodium parasites that cause malaria. To test this, we will use a mouse model of malaria-EBV coinfection in children using the P. yoelii XNL non-lethal model of Plasmodium infection and the MHV-68 model of gammaherpesviruses. The first goal of this research is to identify which cell types produce IL-10 upon co-infection. VertX reporter mice can be used to visualize which cells produce IL-10 via flow cytometry. Here we have also tested iii whether the effects of co-infection can still be seen when the IL-10 gene knocked out specifically in B cells or macrophages, both cells that are infected by MHV-68. |
