Columbia researchers image malaria parasite’s cell-entry anchors
Images of four-protein anchors support a proposed explanation of how the parasite reshapes red blood cell membranes to enter them.
Loading… Բեռնվում է…
Images of four-protein anchors support a proposed explanation of how the parasite reshapes red blood cell membranes to enter them.
Researchers led by Chi-Min Ho at Columbia University have imaged the temporary junction that malaria parasites use to enter red blood cells. Their observations reveal four-protein anchors in detail, providing the structural basis for a proposed explanation of how the parasite reshapes the cell’s membrane, according to Quanta Magazine’s October 23 report.
Scientists already knew that Plasmodium, the single-celled parasite that causes malaria, inserts a ring of protein anchors into a red blood cell’s membrane. The parasite connects to those anchors, passes through the ring and leaves the membrane sealed behind it. This structure is called the moving junction. The entire entry process takes less than a minute, and its small size and brief existence had prevented researchers from seeing its structure clearly.
Ho’s team used cryo-electron microscopy, a method for imaging molecular structures, to examine the four protein components of each anchor. Three proteins injected by the parasite form a dense wedge beneath the red blood cell membrane. A fourth connects that structure to the parasite.
The images establish structural details; the sequence of membrane changes is the researchers’ proposed model. In that model, electrical forces and pressure from many anchors crowd and displace lipids—the molecules that form the membrane. This reverses the membrane’s curvature, making it bow inward around the parasite. Some lipids separate and reassemble into a protective membrane around the invader before the host membrane seals behind it.
Jake Baum, a University of New South Wales parasitologist who was not involved in the research, described the findings as a powerful observation built through successive advances in the field.
The NIH–NASA competition seeks better measurements in laboratory drug-safety models, with submissions scheduled to open on 15 December 2026.
2 min
Entry matters because it allows the parasite to multiply inside red blood cells. Over about 48 hours, the parasites divide until an infected cell bursts, releasing them to invade other cells. Blocking entry could interrupt that cycle.
Ho’s team designed an inhibitory protein targeting the moving junction. In test tubes, it prevented Plasmodium from entering red blood cells. Its safety and efficacy have not been tested in animals, so the result does not establish a treatment.
The speed of invasion also creates a practical difficulty. Keele University molecular parasitologist Christiaan van Ooij noted that some researchers regard invasion as a poor drug target because it is so brief. A drug would have roughly 60 seconds to block entry, meaning it would need to act extremely quickly, remain stable in the body for a long time, or both.
The Simons Foundation partly funded the research and also funds Quanta Magazine. The magazine states that it is editorially independent and that the foundation’s funding decisions do not influence its coverage.
Ho’s team plans to use similar imaging techniques to determine the structures of other protein complexes involved in malaria infection. These include adhesive proteins that help infected red blood cells avoid travelling to the spleen, where defective cells and parasites can be filtered out.
The programme brings together national laboratories, universities and industry partners, with plans for a sensor-equipped test bed and self-adjusting pilot production lines.
2 min
Previously seen only through its infrared heat, the dusty feature is visible in reflected starlight, allowing researchers to test a possible collision origin.
4 min