How drugs beat malaria |
LA TROBE UNIVERSITY |
La Trobe University research has revealed for the first time the mechanism by which current anti-malarial drugs kill the malaria parasite. It also helps us understand how these drugs are developing worrying resistance to a pathogen that kills more than 800,000 children each year. The work has just been published in one of the world’s leading scientific journals, Proceedings of the National Academy of Science (PNAS), in the US. Research team leader, biochemist Professor Leann Tilley, says the research points to new ways of boosting the action of antimalarial drugs to overcome this drug resistance problem. Plasmodium falciparum is the most pathogenic human malaria parasite. It afflicts more than 200 million people world-wide. Treatment relies heavily on combination therapies that include a drug called artemisinin, extracted from the wormwood herb. ‘Recent reports of decreased clinical effectiveness of artemisinin-based drugs are extremely concerning,’ she says. ‘It is therefore critical to understand the way artemisinin works so that we can overcome the pathogen’s resistance to this drug.’ The new work by Professor Tilley and her team shows that artemisinin targets a point of critical vulnerability in the malaria parasite. ‘The parasite invades and grows within the red blood cells of its human victims,’ she says. ‘As it grows it consumes the haemoglobin of the red blood cell and releases an iron-containing pigment, called “haem”.’ Research from her laboratory demonstrates that supplies of this haemoglobin-derived iron are essential if artemisinin is to destroy the parasite. ‘Decreasing the production of this iron renders the parasites resistant to artemisinin,’ Professor Tilley says. ‘We have also shown that the parasite can slow its growth and reduce its haemoglobin uptake rate in response to artemisinin treatment. This helps it avoid the toxic effects of artemisinin.’ Thus the La Trobe study not only gives an important insight into the nature of artemisinin action and resistance, but also suggests that new, longer-lived antimalarials will thwart this resistance mechanism. |
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