Malaria's Achilles' heel foundRed blood cell receptor essential for infection
UK scientists have identified a crucial molecule which the malaria parasite uses to invade red blood cells, new research shows.
Scientists from the Welcome Trust Sanger Institute in Cambridge found that the most deadly species of malaria - Plasmodium falciparum - has to lock on to a single receptor on the surface of red blood cells to gain entry into the cell, where it then continues to multiply.
The discovery of the parasite's "Achilles' heel" raises hope for the development of a vaccine or new treatments for one of the deadliest diseases on the planet.
There is currently no licensed vaccine against malaria, which affects more than 250 million people worldwide. Around one million people die from the disease every year, mostly children under the age of five in sub-Saharan Africa.
The disease is passed on to humans by infected mosquitoes when they feed on human blood. Although the parasites initially hide and multiply in the liver, they soon emerge and enter the bloodstream where they infect red blood cells. It is this stage which is responsible for the symptoms and mortality associated with malaria.
Other studies have identified receptors on red blood cells used by malaria parasites. However, as scientists block one receptor, the parasite switches to another.
The latest study suggests that the latest receptor is essential for the parasite to gain entry into the cell.
Further research by the team showed that interrupting the interaction between the receptor and parasite stopped it from invading the cell.
Dr Julian Rayner, from the Sanger Institute, said: "By identifying a single receptor that appears to be essential for parasites to invade human red blood cells, we have also identified an obvious and very exciting focus for vaccine development.
"The hope is that this work will lead towards an effective vaccine based around the parasite protein."
The study findings are published in the journal Nature.
This article was published on Thu 10 November 2011
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