New Antimalarial Drug Targets Discovered
Researchers have discovered crucial new processes that allow malaria parasites to escape red blood cells and infect other cells, offering potential new treatment targets. The team are already working with pharmaceutical companies to use this knowledge to develop new antimalarial drugs - a critical step in the battle against drug-resistant malaria.
"Over 400,000 people die of malaria each year, and resistance to common antimalarial drugs is growing," says Professor Mike Blackman, Group Leader at the Francis Crick Institute, who led the research. "We're studying the deadliest malaria parasite, Plasmodium falciparum, to try to find new drug targets that work in a different way to existing treatments."
In the latest study, published in Nature Microbiology, the team have identified two key proteins that malaria parasites need to escape red blood cells and infect fresh cells. The research was done in collaboration with the Proteomics Science Technology Platform at the Crick as well as scientists at Birkbeck College, King's College London and the London School of Hygiene & Tropical Medicine.
"We've already started collaborating with GSK to see if designing drugs that target these proteins could form the basis of a new antimalarial drug," says Dr James Thomas, Crick postdoctoral scholar and joint first-author of the paper.
When malaria parasites invade red blood cells, they form an internal compartment where they replicate many times before bursting out of the cell and infecting more cells. In order to escape red blood cells, the parasites have to break through both the internal compartment and the red cell membrane.
The team used genetic knockout experiments to show that a protein called SUB1 is essential for the parasite to break through the internal compartment, while SERA6 - which is activated by SUB1 - is essential for the parasite to break through the red blood cell membrane.
Using analytical tools, the team then figured out how SERA6 breaks through the blood cell membrane. Crick PhD student and joint first-author Michele Tan explains: "There is a strong chicken wire-like meshwork that sits under the red blood cell membrane to provide strength and support. We found that SERA6 cuts the chicken wire, causing the blood cell membrane to collapse and rip open so that the parasites can escape."
This article has been republished from materials provided by the Francis Crick Institute. Note: material may have been edited for length and content. For further information, please contact the cited source.
Kidney Cancer Driver Could Lead to New Treatment StrategyNews
Scientists have uncovered a potential therapeutic target for kidney cancers that have a common genetic change. Scientists have known this genetic change can lead to an overabundance of blood vessels, which help feed nutrients to the tumors. Their latest finding shows a potential new cancer-driving pathway.READ MORE
Targeting Headaches and Tumors with Nano-SubmarinesNews
Scientists have developed a new method to enable miniature drug-filled nanocarriers to dock on to immune cells, which in turn attack tumors. In the future, this may lead to targeted treatment that can largely eliminate damage to healthy tissue.READ MORE
Working Together Helps Phage Overcome CRISPRNews
Surprising results show that phage join forces to overcome bacteria’s CRISPR -based immune defenses. Improved understanding of the interactions between phage and their bacterial hosts could help advance phage-based therapies and stimulate viral research.READ MORE