"This research gives us a new insight into malaria, a major global killer that preys especially on young children and claims a life every 30 seconds," notes Anthony S. Fauci, M.D., director of the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, where the research was conducted.
"If we better understand the natural protective mechanisms against malaria, we might be able to mimic that protective effect through vaccines or drugs," says NIAID researcher Thomas E. Wellems, M.D., Ph.D., whose team's findings appear this week in the journal Nature.
Hemoglobin exists in several varieties. Hemoglobin A is the most common, but in parts of West Africa, where malaria is rife, one-fourth of the population has at least one gene for hemoglobin C. Children with at least one hemoglobin C gene are less prone to deadly cerebral malaria, in which parasite-infected red blood cells accumulate in the brain. But how hemoglobin C confers this protection has puzzled scientists until now.
To solve the mystery, Dr. Wellems and his colleagues studied laboratory-infected red blood cells and blood drawn from children with malaria from the African nation of Mali. Genetically, the samples fell into three groups: those with two genes for hemoglobin A (AA); those with two genes for hemoglobin C (CC); or those with one gene for each type of hemoglobin (AC).
The scientists then measured three phenomena that affect how well parasitized red blood cells can be made to stick to one another, to uninfected red blood cells and to blood vessel walls. These phenomena--known respectively as aggl
Contact: Anne A. Oplinger
NIH/National Institute of Allergy and Infectious Diseases