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Scientists have sequenced the genome of one of the parasites that causes elephantiasis, a move that could lead to new drug targets for the disease.

The research, from the United Kingdom, United States and Canada, was published in Science last week (21 September). It compares the genome of Brugia malayi, a parasitic worm, with those of two other organisms to identify genes specifically associated to parasitism.

Elephantiasis, or lymphatic filariasis, is a mosquito-borne disease caused by several types of nematode worm, including B. malayi. It affects 100 million people, mostly in the developing world, according to the WHO.

Once a person is infected, the parasite resides in the body's lymph nodes resulting in swelling and the deformed growth of limbs and genitals.

Although available treatments are effective, they need long-term courses and patient adherence tends to be low, compromising their efficiency. The drugs also have toxic side effects and cases of drug resistance have been reported, highlighting the need for new therapies.

The researchers identified 11,500 protein-coding genes in B. malayi. Elodie Ghedin, from the US-based Pittsburgh School of Medicine and lead author of the paper told SciDev.Net that the research team was surprised to find that when comparing B. malayi genes with previously sequenced genes, about 20–30 per cent had no match.

Some of the predicted proteins for these new genes appear to be similar to known immuno-modulator proteins — regulators of the immune system — suggesting that they are involved in deactivating the host's immune system to ensure the parasite remains undetected.

"This worm can reside in the host for years and not necessarily cause disease, in fact the less disease the individual has, the more worms there are in circulation," says Ghedin. "Now that we know those genes don't exist in humans we can target them to control disease."

She added that knowledge of these previously unknown immune suppressors could also be of use in organ transplants and to help treat autoimmune disease.

Link to full paper in Science

Reference: Science, 317, 1756 (2007)

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