CAMBRIDGE, Mass.--During the first 24 hours of invasion by the malaria-inducing parasite Plasmodium falciparum, red blood cells start to lose their ability to deform and squeeze through tiny blood vessels-one of the hallmarks of the deadly disease that infects nearly 400 million people each year. Now, an international team of researchers led by an MIT professor has demonstrated just why that happens.

By knocking out the gene for a parasite protein called RESA (ring-infected erythrocyte surface antigen), the researchers found that the protein, transferred from the parasite to the cell's interior molecular network, causes red blood cells to become less deformable.

"This is the first time a particular protein has been shown to have such a large effect on red blood cell deformability," said Subra Suresh, Ford Professor of Engineering and senior author of a paper on the work appearing in the online edition of the Proceedings of the National Academy of Sciences the week of May 21.

The work, a collaboration between researchers at MIT, the Institut Pasteur in Paris, France and the National University of Singapore, could ultimately lead to the development of treatments that target the parasite protein.

Suresh, who holds appointments in materials science and engineering, biological engineering, mechanical engineering and the Harvard-MIT Division of Health Sciences and Technology, has been studying the mechanics of red blood cells and the effects of malaria on those cells for several years.

When the malaria parasite, Plasmodium falciparum, infects red blood cells, the blood cells lose their ability to deform and eventually clump together and get stuck in tiny blood vessels, or capillaries.

The RESA protein has long been suspected to be involved in the early stages of that process. The parasite produces RESA during the first stage of malaria (known as the ring stage) and then transports it to the cell surface.