Analysis of exported proteins and parasite-induced host cell rigidity changes during the Plasmodium falciparum intraerythrocxytic life cycle

Malaria is an infectious disease of global public health importance. Despite a number of successful efforts to fight the disease, there are still over 200 million cases and 445,000 deaths each year. Plasmodium falciparum, a protozoan parasite, is the causative agent of severe malaria. The parasite is transmitted by female Anopheles mosquitos form human to human and has different life stages inside both hosts. However, the only stages that are accountable for clinical symptoms of the disease are asexually replicating stages in the red blood cells. Red blood cells are highly specialized cells lacking a nucleus, organelles and certain cellular mechanisms. Therefore, the parasite has to extensively remodel the erythrocyte to ensure survival. The remodeling is achieved by exporting a large number of proteins that have various functions. Those functions include nutrient uptake and host immune response evasion.