A form of malaria common in India, Southeast Asia and South America attacks human red blood cells by clamping down on the cells with a pair of proteins, new research at Washington University School of Medicine in St. Louis has revealed.
The study provides details that will help scientists design better vaccines and drug treatments for the strain, Plasmodium vivax.
"More people live at risk of infection by this strain of malaria than any other," said senior author Niraj Tolia, PhD, assistant professor of molecular microbiology and of biochemistry and molecular biophysics. "We now are using what we have learned to create vaccines tailored to stop the infectious process by preventing the parasite from attaching to red blood cells."
The finding appears Jan. 9 in PLOS Pathogens.
The World Health Organization estimates there were more than 200 million malaria cases in 2012. The deadliest form of malaria, Plasmodium falciparum, is most prevalent in Africa. But P. vivax can hide in the liver, re-emerging years later to trigger new infections, and is harder to prevent, diagnose and treat.
Earlier studies had suggested that one P. vivax protein binds to one protein on the surface of red blood cells. Tolia's new study reveals that the binding is a two-step process that involves two copies of a parasite protein coming together like tongs around two copies of a host protein.
"It's a very intricate and chemically strong interaction that was not easily understood before," Tolia said. "We have had hints that other forms of malaria, including the African strain, may be binding in a similar fashion to host cells, but this is one of the first definitive proofs of this kind of attack."
Tolia suspects blocking any of the proteins with drugs or vaccines will stop the infectious process.