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Fat-free proteins kill tropical disease bug

13 April 2010

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Category: Research & medical benefits

lab–mouse.jpgParasites which cause sleeping sickness can be killed by altering the proteins that they are dependent on, studies on mice show.

The disease is caused by the parasite T.Brucei which has many similarities with human host cells. Yet it evolved some unique characteristics which make for possible targets for a new treatment. Scientists found that the parasite relies on the fatty acids attached to proteins for its survival. So they developed a drug that inhibits the enzyme NMT which is involved in the addition of fatty acids to proteins.

When NMT is inhibited, the parasite can no longer make use of the fatty acids attached to proteins, and eventually dies. Researchers saw this effect in mice that were given low doses of the treatment. The medicine is exciting because it can be taken orally, and has much milder side effects than current arsenic-based treatments. However it was only effective in mice before stage 2 of the virus when the parasite invades the host's nervous system. The drug may also be dangerous in higher doses needed for the human treatment of the disease.

The team of scientists wish to continue targeting other enzymes crucial to the parasite's survival. This study in particular has been important in highlighting the need for effective medicines which have all the desired characteristics and no side effects. The team think the treatment will be ready for clinical trials in around 18 months time.

Sleeping sickness, also known as Human African tripanosomiasis, is one of the neglected tropical diseases which affect some of the world's poorest populations. The fatal illness infects tens of thousands of Africans each year. One of the challenges the team of scientists therefore face is trying to engage big pharmaceutical companies to invest in future treatments for these devastating diseases.