Plasmodium falciparum, the most lethal malaria parasite, is a housebreaking villain of the red blood cell world. Like a burglar searching for a way in to his targeted premises, the parasite explores a variety of potential entry points to invade the red blood cells of its human victims. When a weak point is found, the intrusion proceeds.
Scientists have known about the parasite's housebreaking habit for a decade, but just how it breaks in to blood cells has been unknown.
Now, an international team of scientists, led by WEHI's Professor Alan Cowman, has discovered the gene - known as PfRh4 - that the parasite uses as a tool to switch between potential invasion points. More specifically, the gene provides the parasite with the ability to switch from receptors on red blood cells that contain sialic acid to those that do not.
In effect, if the gene finds all the doors locked, then it will try all the windows until it finds one it can force open.
The team who performed the research work consisted of Janine Stubbs, Ken Simpson, Tony Triglia, David Plouffe, Christopher J. Tonkin, Manoj T. Duraisingh, Alexander G. Maier and Elizabeth Winzeler. Professor Cowman and his team at WEHI worked with researchers from the Scripps Research Institute (TSRI) in La Jolla, California and the Genomics Institute of the Novartis Research Foundation in San Diego, California.
This discovery made by the group will have a profound impact upon the design of new anti-malarial vaccines, since the inactivation of this single protein could block multiple entry points currently open to the parasite.
Professor Cowman is a Howard Hughes Medical Institute international research scholar. The results of the new study are published in the 26 August 2005 issue of the prestigious journal, Science.
Source: Eurekalert & othersLast reviewed: By John M. Grohol, Psy.D. on 21 Feb 2009
Published on PsychCentral.com. All rights reserved.
It is hard to fail, but it is worse never to have tried to succeed. In this life we get nothing save by effort.
~ Theodore Roosevelt