Gene discovery offers potential for new sleeping sickness treatment

15 May 2009

A newly discovered set of genes could help limit the transmission and impact of sleeping sickness, according to a Trust-funded study.

The genes, identified by scientists at the University of Edinburgh and the University of Canberra, Australia, play a role in the replication of the sleeping sickness parasite, and could form a target for future therapies.

"Our findings pinpoint a set of genes that could help make this parasite much less harmful to people and animals," said Professor Keith Matthews from the University of Edinburgh, who led the study.

"We hope this will lead to a search for therapies that can limit the impact of this parasite or prevent the spread of sleeping sickness."

Sleeping sickness, or human African trypanosomiasis, is caused by the parasite Trypanosoma, which infects the bloodstream of people and animals and is spread by the blood-sucking tsetse fly.

The parasite exists in two forms: a slender form, adapted for replicating in a mammalian bloodstream, and a stumpy form, modified for multiplication in the fly and easier for flies to carry.

In the study, researchers found a set of genes that tell the parasite when it has been taken up by a feeding fly. The discovery will allow scientists to more easily distinguish between the two forms of the parasite, which could lead to better monitoring and modelling of disease transmission.

Furthermore, the researchers showed that blocking the genes makes stumpy-form parasites less responsive to the signals that trigger the parasite to multiply. Potentially, scientists could develop drugs that mimic this process, forcing the parasite to exist only in its stumpy form and making the disease less harmful. A milder form could prevent some of its symptoms and allow the patient's immune system to clear the infection.

Sleeping sickness is endemic in sub-Saharan Africa, where it affects between 50 000 and 70 000 people, according to the World Health Organization. If left untreated, the parasite disrupts the central nervous system and is fatal.

Image: A high-power scanning electron micrograph of Trypanosoma brucei brucei parasites at the procyclic stage, from the mid-gut of a tsetse fly. Gull Lab, Sir William Dunn School of Pathology, Wellcome Images

Reference

Dean S et al. A surface transporter family conveys the trypanosome differentiation signal. Nature 2009;459:213-7.