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Blocking an essential nutrient inhibits malaria parasite growth

While very much in its infancy, the results could open the door to a new way to fight malaria.

More than 90 percent of the Aedes aegypti mosquitoes tested in Cambodia showed 'an extremely high level of resistance' to insecticides, a new study shows
More than 90 percent of the Aedes aegypti mosquitoes tested in Cambodia showed 'an extremely high level of resistance' to insecticides, a new study shows - Copyright Courtesy of Shinji Kasai/AFP SHINJI KASAI
More than 90 percent of the Aedes aegypti mosquitoes tested in Cambodia showed 'an extremely high level of resistance' to insecticides, a new study shows - Copyright Courtesy of Shinji Kasai/AFP SHINJI KASAI

Virginia Tech researchers in the College of Agriculture and Life Sciences found that by preventing the malaria parasite from scavenging fatty acids, a type of required nutrient, it could no longer grow.

This parasite has affected an estimated 249 million people in 2022. Malaria occurs while the parasite is replicating in human red blood cell and it relies on scavenging, rather than creating, to satisfy its need for fatty acids.

According to lead researcher Michael Klemba: “The key to this breakthrough is that we were able to develop a screening method for the malaria parasite and block this process.”

Klemba adds: “While very much in its infancy, the results could open the door to a new way to fight malaria.”

To reach this conclusion, researchers undertook experiments with infected red blood cells and found chemicals that can stop the parasite from getting the needed fatty acids. It was next discovered that two enzymes were instrumental in breaking down host lipids to release the fatty acids the parasite needs. These enzymes work in different places: One works outside in the red blood cell, and the other works inside the parasite.

The scientists found that when they removed these two enzymes, they detected that the parasite struggled to get the needed fatty acids and couldn’t grow well. This was especially true when that host lipid was the only fatty acid source available. When both enzymes were stopped from working, either by changing the parasite’s genes or by using drugs, the parasites couldn’t grow in human blood.

This experiment reveals that breaking down the host lipid, called lysophosphatidylcholine, to get fatty acids is critical for the malaria parasite’s survival in our bodies and that targeting these two enzymes could be a new way to fight malaria.

Earlier work shows that when lysophosphatidic acid levels drop in the host that the malaria parasite – Plasmodium falciparum –  converts into a form that can be taken up by mosquitoes. P. falciparum causes malaria while replicating in host erythrocytes (red blood cells) and relies on scavenging rather than synthesis, or the creation of compounds, to satisfy its need for fatty acids.

Of the two enzymes important for this process: one is inside the parasite, and the other is exported into the host cell. This is not typical of metabolic processes as they are typically carried out within the parasite.

The researchers found that only removing one of the two enzymes, which they named XL2 and XLH4, does not do anything. Both have to be removed to inhibit parasitic growth.

The research has been published in the journal Proceedings of the National Academy of Sciences of the United States of America. The research paper is titled “Metabolism of host lysophosphatidylcholine in Plasmodium falciparum–infected erythrocytes.”

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Written By

Dr. Tim Sandle is Digital Journal's Editor-at-Large for science news. Tim specializes in science, technology, environmental, business, and health journalism. He is additionally a practising microbiologist; and an author. He is also interested in history, politics and current affairs.

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