Even though the most deadly form of malaria for humans, Plasmodium falciparum, has been linked to malaria found in chimpanzees, this group has been fairly isolated on the malarial family tree—until now.

About 2 million people die of malaria every year, of which more than a million are children in sub-Saharan Africa. Malaria is caused by a protozoan parasite belonging to the genus Plasmodium, and Plasmodium falciparum is responsible for the most severe form of malaria.

Funded by a $1.5 million grant from the National Institutes of Health, scientists at Binghamton University, State University of New York, hope to understand how the malaria parasite Plasmodium falciparum evolved resistance to the once-effective medication chloroquine.

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.

Passive immunization through the development of fully human antibodies specific to Plasmodium falciparum may be effective at controlling the disease, report researchers led by Dr. Richard S. McIntosh from the University of Nottingham in a paper published this week in the open-access journal PLoS Pathogens. The researchers developed these novel reagents by antibody repertoire cloning generated from immune Gambian adults.

Scientists at CNRS and the Pasteur Institute, collaborating with physicians in Gabon, have just undertaken a study on cerebral malaria in children living in an endemic region. This study, which was published in PLoS ONE, should allow us to better understand this severe form of malaria which affects 20 to 40 percent of people infected by the Plasmodium falciparum parasite, and is fatal in 30 to 50 percent of cases.