Funding outcome

Malaria is caused by infection with a parasite. Significant pathology occurs, especially when red blood cells are infected. Pregnant women are particularly susceptible where parasites can accumulate in the placenta. This poses a major threat to both mother and fetus, leading to higher chances of fetal mortality and poor birth outcomes. Placental malaria occurs because the parasite produces a specific protein on the surface of the infected red blood cell (iRBC) which binds to a receptor only found on the placenta. High numbers of iRBCs bind to the placenta causing pathology. Women who are infected with malaria over several pregnancies develop protective factors called antibodies that stop the binding of iRBCs to the placenta. This prevents placental malaria and leads to healthier babies. Our strategy is to develop a vaccine that will produce the same antibodies to prevent parasites from binding to the placenta. However, current lab assays used to test the blocking function of these antibodies do not adequately mimic the way parasites bind to the placenta in pregnant women. This makes it difficult to gauge the efficacy of vaccines that are currently in human clinical trials or identify new promising vaccine candidates in the lab. This project will develop a new tissue-based model of placental malaria using human term placentas. I will quantify parasite binding through detection of different markers on placenta tissue and parasites. I will then test blocking of this binding using antibodies isolated from individuals infected with malaria. Once optimized, this new model will be applied to test vaccine candidates to support successful vaccine development.