Discovery of key malaria proteins could mean sticky end fo...( Scientists funded by the Wellcome Tr...),Health

Scientists funded by the Wellcome Trust have identified a key mechanism that enables malaria-infected red blood cells to stick to the walls of blood vessels and avoid being destroyed by the body's immune system. The research, published today in the journal Cell, highlights an important potential new target for anti-malarial drugs.

Malaria is one of the world's biggest killers, killing over a million people every year, mainly children and pregnant women in Africa and south east Asia. It is caused by the malaria parasite, which is injected into the bloodstream from the salivary glands of infected mosquitoes. There are a number of different species of parasite, but the deadliest is the Plasmodium falciparum parasite, which accounts for 90% of deaths from malaria.

The malaria parasite infects healthy red blood cells, where it reproduces, producing up to thirty-two new daughter parasites. The parasite secretes a "glue", known as PfEMP1, which travels to the surface of the infected red blood cells, leading to the formation of the knobs on the surface of the cells. The cells become sticky and adhere to the walls of the blood vessels. This prevents the cells being flushed through the spleen, where the parasites would be destroyed by the body's immune system, but also restricts blood supply to vital organs.

Now, an international collaboration of scientists has identified eight new proteins that transport the P. falciparum parasite's "glue" to the surface of the infected red blood cells. The researchers, led by Professor Alan Cowman from the Walter and Eliza Hall Institute of Medical Research in Melbourne, Australia, have shown that removing just one of these proteins prevents the infected red blood cells from sticking to the walls of the blood vessels.

"These findings greatly enhance our understanding of how the malaria parasite commandeers the red blood cell for its own survival and avoids our immune defences," says Pr
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