The investigators, led by Kasturi Haldar and N. Luisa Hiller, also found that the process by which the malarial parasite remodels red blood cells is far more complex than scientists previously had realized.
Haldar is Charles E. and Emma H. Morrison Professor in Pathology and professor of microbiology-immunology and Hiller a sixth-year student in the Integrated Graduate Program in the Life Sciences at Northwestern University Feinberg School of Medicine.
Other key researchers on this study were Souvik Bhattacharjee; Christiaan van Ooij; Konstantinos Liolios; Travis Harrison; and Carlos Estrano.
Findings from the Northwestern study were published in the Dec. 10 issue of the journal Science.
Malaria is a blood-borne illness transmitted by mosquitoes. Forty percent of the world's population lives at risk for infection, and between 200 and 300 million people are afflicted each year, particularly in underdeveloped and impoverished tropical and sub-Saharan countries.
Plasmodium faciparum is the most virulent form of the four human malarial parasite species, killing over 1 million children each year, and is responsible for 25 percent of infant mortality in Africa, according to the World Health Organization.
Following invasion of human red blood cells the "blood stage" of malaria P. falciparum exports proteins that modify the properties of the host red blood cell membrane, are required for parasite survival and are responsible for fatal pathologies such as cerebral or "brain" malaria as well as placental malaria.
It is during the "blood stage" of malaria when symptoms of malaria occur. These symptoms include fever and flu-like symptoms, such as chills, headache, musc
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