The mechanism by which the deadly species of malaria parasite, Plasmodium falciparum invades human red blood cells has been discovered by scientists.
They have found that the parasite relies on a single receptor on the red blood cell's surface to invade, offering an exciting new focus for vaccine development.
The blood stage of Plasmodium's lifecycle begins when the parasite invades human red blood cells, and it is this stage that is responsible for the symptoms and mortality associated with malaria.
Researchers have tried for many years to develop a vaccine to prevent the parasite gaining entry into our red blood cells, but so far they have been unsuccessful.
"Our findings were unexpected and have completely changed the way in which we view the invasion process," said Dr Gavin Wright, senior co-author from the Wellcome Trust Sanger Institute.
"Our research seems to have revealed an Achilles' heel in the way the parasite invades our red blood cells. It is rewarding to see how our techniques can be used to answer important biological problems and lay the foundations for new therapies," he stated.
The interaction between the parasite protein and the host receptor was discovered using a technique called AVEXIS (Avidity-based Extracellular Interaction Screen).
As well as identifying the interaction, the researchers demonstrated that disrupting this interaction completely blocked the parasite from gaining entry into the red blood cell.
Importantly, this was true across all parasite strains tested, making it appear that the receptor is a universal entry pathway. It is hoped that the parasite's dependency on this one protein can now be exploited to develop new and effective vaccines.