Host red blood cell modification sustains the virulence of malaria parasites

Image: Plasmodium falciparum (green) normally exports proteins (red) into its human erythrocyte host cells using the PTEX complex (upper left). Genetic attenuation of PTEX prevents export into the host cells leaving the exported proteins trapped around the parasite periphery (lower right).

Malaria kills more than half a million people in tropical countries every year where nearly half the world’s population live.

Malaria is caused by parasites that are spread from person to person by mosquito bite. The parasites infect and destroy our red blood cells, thereby making us very sick. The disease is particularly severe in young children and can even be fatal.

The potential of malaria parasites to do harm relies of their ability to modify their human host cells. By understanding how this happens we can develop new anti-malaria therapies.

Parasites have become resistant to many existing medicines so new ones have to be invented. The ability of parasites to grow quickly and to hide from our immune systems is due to their potential to renovate their host red blood cells by exporting effector proteins into them.

Recently we discovered molecular gateways called PTEX, that surround the parasites and help courier the exported proteins into their red blood cells. We found that when we stopped the parasites from making the PTEX gateways they rapidly died. We are now trying to develop new medicines that act like a plug to block the PTEX gateways thereby killing the parasites and curing the patient.







Health Issue

Contact Details

For any general enquiries relating to this project, please contact:

Associate Professor Paul Gilson

Deputy Discipline Head, Life Sciences; Co-Head, Malaria Virulence and Drug Discovery Group; Head of Burnet Cell Imaging Facility