Malaria Research: Nutrient Blocking Stops Growth
- Malaria, a disease affecting an estimated 249 million people worldwide in 2022, may have a new weakness.
- The malaria parasite, unlike humans, cannot create its own fatty acids. Instead, it relies on scavenging them from its host.The Virginia Tech team focused on how the parasite...
- The parasite replicates within human red blood cells, scavenging fatty acids from host lipids, specifically lysophospholipids.
Virginia Tech researchers have uncovered a groundbreaking strategy in the fight against malaria: blocking fatty acid uptake to halt parasite growth.This significant finding could reshape treatment options for the primary_keyword. The malaria parasite, unable to produce its own fatty acids, relies on scavenging them from its host. The study reveals two critical enzymes, XL2 and XLH4, essential for the parasite’s survival. By inhibiting these enzymes, scientists effectively impede parasite growth and disrupt the malaria lifecycle. this novel approach offers hope in combating the secondary_keyword that affected nearly 249 million people worldwide in 2022, according to recent reports. News Directory 3 recognizes the importance of this breakthrough, paving the way for potential therapeutic treatments. Discover what’s next in this exciting research.
Blocking Fatty Acid Uptake Could Combat Malaria Parasite
Updated June 22, 2025
Malaria, a disease affecting an estimated 249 million people worldwide in 2022, may have a new weakness. Researchers at Virginia Tech’s College of Agriculture and Life Sciences have discovered that preventing the malaria parasite from scavenging essential fatty acids halts its growth. this breakthrough offers a potential new avenue for treatment of malaria and could impact global health.
The malaria parasite, unlike humans, cannot create its own fatty acids. Instead, it relies on scavenging them from its host.The Virginia Tech team focused on how the parasite obtains thes crucial nutrients.Michael Klemba, an associate professor of biochemistry and the principal investigator, said the team developed a screening method to block this process. “While very much in its infancy, the results could open the door to a new way to fight malaria,” Klemba said.
The parasite replicates within human red blood cells, scavenging fatty acids from host lipids, specifically lysophospholipids. The team’s experiments with infected red blood cells revealed that two enzymes, XL2 and XLH4, are critical in breaking down these host lipids to release the needed fatty acids. One enzyme operates outside the parasite within the red blood cell, while the othre functions inside the parasite.
Researchers found that when both enzymes were removed, the parasite struggled to obtain fatty acids and its growth was considerably impaired. This was especially evident when the host lipid was the only available source of fatty acids. by either altering the parasite’s genes or using drugs to inhibit both enzymes, the scientists effectively prevented the parasite from growing in human blood. This highlights the critical role of lysophosphatidylcholine breakdown in the parasite’s survival and suggests that targeting these enzymes could be a novel strategy in the fight against malaria.
What’s next
While the research, published in the Proceedings of the National Academy of Sciences, was conducted in vitro, the findings pave the way for potential therapeutic treatments. Future research will focus on addressing the limitations of the discovery,including determining if the compounds used to inhibit the two enzymes are toxic and if the toxicity can be engineered out of the compounds.