The malaria type 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 found.
The study provides details that will help scientists design better vaccines and drug treatments for the strain, Plasmodium vivax, researchers said.
"More people live at risk of infection by this strain of malaria than any other," said senior author Niraj Tolia, assistant professor of molecular microbiology and of Biochemistry and molecular biophysics.
P vivax can hide in the liver, re-emerging years later to trigger new infections, and is harder to prevent, diagnose and treat, researchers said.
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.
"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," said Tolia.
Tolia suspects blocking any of the proteins with drugs or vaccines will stop the infectious process.
"For example, some people have a mutation that eliminates the protein on red blood cell surfaces that P vivax binds to, and they tend to be resistant to the parasite," he said.
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