A mutation on the surface of human red blood cells provides protection against malaria caused by the parasite Plasmodium vivax, research led by Case Western Reserve University School of Medicine shows.
The minute change, at a single position of red blood cell surface protein called the Duffy blood-group antigen, has been known for years. But the researchers found this difference makes it harder for the parasite to lock onto the cell and gain entry.
No entry, no infection.
The research is now published online in the Early Edition of the Proceedings of the National Academy of Sciences.
"The finding has practical implications as medical researchers continue attempts to develop a vaccine for vivax malaria," said Christopher King, a professor of international health, medicine and pathology at the Center for Global Health and Diseases at Case Western Reserve University School of Medicine, and lead author.
The protective aspect of the mutation was discovered in campus labs and confirmed through a population study in the Amazon region of Brazil.
Malaria is caused by four different parasites; the majority of cases in Asia and the Americas are caused by P. vivax.
"Plasmodium vivax carries a Duffy binding protein that binds to the Duffy antigen on the surface of the red cell, a critical step to invading the cell," Dr. King explained. "Both parasite and human proteins appear to be needed for the parasite to invade the cell."
King's lab had been studying the parasite's protein, as a target for a vaccine. He teamed with Peter A. Zimmerman, a professor of international health, genetics and biology, also at the Center for Global Health and Diseases. Zimmerman's lab was studying the mutation in the DNA sequence of Duffy blood group gene.
While investigating the binding process, they found that Duffy binding protein interaction with red blood cells varied between samples.
|Contact: Kevin Mayhood|
Case Western Reserve University