Malaria parasites hijack human red blood cells by commandeering the cells' own proteins, but scientists do not know exactly which proteins are involved. This matters because *Plasmodium falciparum* kills hundreds of thousands of people each year. The parasite hides inside red blood cells, remodelling them to survive while evading the immune system. Without a precise map of which human proteins the parasite exploits, drug designers cannot target the weak points. This project will build that map. Researchers will identify every interaction between parasite and host proteins during remodelling, then zoom in on key interactions to see how human proteins change shape when taken over. They will also develop a new method to watch these interactions happen inside living red blood cells. If successful, the work will give medicinal chemists a clear set of molecular targets. That could lead to drugs that block the parasite's ability to remodel red blood cells, stopping the infection before it becomes severe. The research is fundamental—it does not promise a new drug tomorrow—but understanding exactly how the parasite commandeers its host is the necessary first step toward designing one.
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Malaria is an acute disease caused by the parasite Plasmodium Falciparum, which is directly responsible for hundreds of thousands of deaths per year. Plasmodium Falciparum enters the human bloodstream when an infected mosquito penetrates the skin. The parasite then penetrates red blood cells and makes its home inside them. Here, it can hide from the human immune system whilst creating a place for it to survive. This process is often referred to as remodeling. The parasite's remarkable ability to evade the human immune system is what makes it so challenging to eradicate or design new therapeutics against it. Despite its clear importance the details of how Plasmodium Falciparum remodels the red blood cell is still unclear how it does this. We already know that the parasite uses some of the red blood cells' own proteins to carry out the necessary functions but do not have a precise understanding of which ones. It is important to understand which proteins the parasite is using so we can design drugs to stop it in its tracks. Firstly, this research will generate a "map" of interactions between the parasite and the host human cells whilst the parasite is remodeling the red blood cells for its purposes. Secondly, key interactions need to be understood in more detail and we will use other methods to see how human proteins change shape when they are used by the parasite. This will give us key insights into how they function. Finally, we will develop a new method that will allow us to examine how these interactions are changing inside the red blood cells. Together these data will provide us a new understanding of the remodeling process. In particular, it will inform medicinal chemists how to design new drugs against the malaria parasite.
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