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Scientists identify motor that powers parasitic cell invasion

The development of drugs to combat some of the world's most serious parasitic diseases is a step nearer with the discovery of a widely-shared gene that helps parasites to invade host cells.

The new understanding of the gene's role in the single-celled parasite Toxoplasma gondii gives scientists a target to block that could stop the parasite literally in its tracks.

In experiments reported today in the journal Science, researchers at Imperial College London and the University of Mannheim, Germany show that the motor powering Toxoplasma's invasion of host cells is stopped when the parasite myosin A gene is disrupted.

Myosin A is present in all members of the Apicomplexa family of parasites, which includes Toxoplasma and Plasmodium falciparum, which cause Toxoplasmosis and malaria respectively.

Toxoplasma, mainly transmitted by consumption of contaminated meat or by cat faeces, chronically infects half the world's population. The pathogen is a leading cause of neurological birth defects in children born to mothers who contract the disease during pregnancy and can cause fatal toxoplasmosis encephalitis in immunosuppressed patients.

Scientists hope that understanding the gene's function will aid efforts to develop drugs that target and block the way Apicomplexa parasites penetrate host cells.

Unlike most viruses and bacteria that require host cell participation to attack cells and be engulfed, Apicomplexans actively penetrate cells.

They use a unique gliding motion powered by an actin-myosin system to rapidly spread throughout tissues in the host's body and to invade cells.

"Our research demonstrates for the first time that parasite motility is powered by an unusual motor, which is essential for invading host cells," says research leader Dr Dominique Soldati from Imperial's Department of Biological Sciences.

"The Apicomplexa family of parasites are all strictly dependent on an unusual gli
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Contact: Judith H Moore
j.h.moore@ic.ac.uk
44-207-594-6702
Imperial College London
24-Oct-2002


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