New York: Researchers have found that the deadliest malaria parasite needs two proteins to infect red blood cells and exit the cells after it multiplies, a finding that may help develop potential new drug targets.
Plasmodium falciparum, the species of parasite that causes the most malaria deaths worldwide, has developed drug-resistance in five countries in Southeast Asia.
The study, led by Armiyaw S. Nasamu, from the Washington University School of Medicine-St. Louis, focussed on the role of plasmepsins IX and X -- two of the 10 types of plasmepsin proteins produced by P. falciparum for metabolic and other processes.
The researchers created malaria parasites that lacked plasmepsin IX or X under experimental conditions and compared them to those that had the two proteins.
The results appearing in the journal Science, showed that parasites lacking plasmepsin IX had defective rhoptries -- specialised cell structures inside the parasite that help in invading red blood cells.
Further, when the parasites are deprived of plasmepsin X, they could not process a protein called SUB1 as well as infect the red blood cells or exit these cells after multiplying.
The parasites lacking the plasmepsins could potentially be used to screen candidate drugs to identify additional anti-malaria compounds, the researchers noted.
Moreover, the researchers also identified three experimental malaria drugs that may work by targeting plasmepsin X.
One drug, called CWHM-117, has already been tested in a mouse model of malaria.
The new findings may help researchers modify CWHM-117 to make it more effective, the researchers said.