Red blood cell mutation can protect against malaria

A new study has shown that a mutation on the surface of human red blood cells can provide protection against malaria caused by the Plasmodium vivax parasite.

Research by scientists at Case Western University School of Medicine demonstrated that a tiny change in the position of a red blood cell surface protein called the Duffy blood-group antigen makes it significantly more difficult for the parasite to hook onto the cell and then gain entry into it. Without entry into the cell, no infection can occur.

"The finding has practical implications as medical researchers continue attempts to develop a vaccine for vivax malaria," Dr. Christopher King, a lead author of the study and a professor of international health, medicine and pathology at Case Western Reserve University of Medicine, said.

The mutation’s protective properties were discovered in laboratories on campus and confirmed through a population study performed in the Amazon region of Brazil. The study appears in the early edition of the Proceedings of the National Academy of Sciences.

"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," King said. "Both parasite and human proteins appear to be needed for the parasite to invade the cell."

King was investigating the binding process with Peter A. Zimmerman at Case Western when they found that the protein interaction varied between samples. P. vivax bound to the blood cell samples with the mutation approximately half as often as they did with those that did not express the mutation.

To determine whether or not their findings could be observed among a general population, the researchers collaborated with Marcelo Ferreira at the University of Sao Paulo. Together, they tracked approximately 400 individuals for more than a year in northwestern Brazil. Their results have led them to believe that the mutation became more commonplace specifically because it protects against P. vivax.

The researchers found no relationship between the mutation and Plasmodium falciparum, the parasite that causes the majority of malaria infections in sub-Saharan Africa.