LEICESTER, England, July 7 (UPI) -- Researchers have identified one of the proteins that allows the parasite that causes malaria to enter red blood cells and prevented it from doing so in lab tests, potentially paving a path toward new drugs to treat the disease.
The study was focused specifically on dissecting the biochemical pathways the parasite uses to stay alive, including the use of synthetic chemicals used in combination with changes to its DNA.
"This is a real breakthrough in our understanding of how malaria survives in the blood stream and invades red blood cells," said Andrew Tobin, a professor at the University of Leicester, in a press release. "We've revealed a process that allows this to happen and if it can be targeted by drugs we could see something that stops malaria in its tracks without causing toxic side-effects."
Among several proteins important to the survival of malaria, researchers found that when they blocked the protein kinase PfCDPK1, it prevented the parasite from entering cells. This causes the parasite to die because it can't enter cells and live off of them.
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By identifying this key protein kinase, researchers said future drugs can be tailored to focus on PfCDPK1 without toxic side effects for healthy patients, and also safe enough for pregnant women and children.
"Tackling malaria is a global challenge, with the parasite continually working to find ways to survive our drug treatments," said Patrick Maxwell, a professor at the University of Leicester. "By combining a number of techniques to piece together how the malaria parasite survives, this study opens the door on potential new treatments that could find and exploit the disease's weak spots but with limited side-effects for patients."
Malaria, caused by a parasite that lives in mosquitoes and is spread by their bite, infects more than 200 million people per year and is responsible for over 500,000 deaths per year, according to the World Health Organization.
The study is published in Nature Communications.
