The most severe form of malaria, a disease that affects over 300 million people annually, is caused by the single-celled parasite plasmodium falciparum, which was the focus of the study.
A number of different proteins on the surface of malaria parasites help the invaders bind to red blood cells. But once attached to host blood cells, the parasites need to shed the ‘sticky’ surface proteins that would otherwise interfere with entrance into the cell.
“What we have discovered is the parasite enzyme – we refer to it as a ‘sheddase’ – which sheds the sticky proteins,” says Michael Blackman, senior author of the study and parasitologist at London’s National Institute for Medical Research. The enzyme is required for the parasites to invade cells; without it, the parasites die.
The enzyme is stored in and released from cellular compartments near the tip of the parasite, according to the study. Once on the surface, the enzyme attaches to a motor that shuttles it from front to back, liberating the sticky surface proteins. With these proteins removed, the parasite gains entrance into a red blood cell. The entire invasion lasts about 30 seconds.
By designing a specific inhibitor that impeded the ability to shed the sticky proteins, Mr Blackman and his team interfered with the enzyme’s normal functioning. A drug (yet to be designed) could possibly do the same, preventing the parasites from infecting blood cells.