One of the banes of modern medicine is that if there’s no money in the treatment, then there is no treatment. The plight of erectile dysfunction in the industrialized world takes precedent over African sleeping sickness. With any luck, in light of recent events, times they may be a-changing.
The discovery of 6,200 genes shared by a collection of parasites known as trypanosomes, or Tritryps, is encouraging the hopes of finding a common treatment for all three of the diseases spread by small insects like the tsetse fly, bloodsucking triatomine bugs, and the sand fly.
“It’s a major milestone for all of us, and the first big step towards finding solutions to these diseases,” says geneticist Najib El-Sayed of the Institute for Genomic Research in Rockville, Maryland, who is among several leading researchers whose work was published in Science.
While medicine designed to target the genome sequences of the parasites is already a precise endeavor, researchers say they need to identify even more picayune details of the sequence to separate those genomes also shared by humans.
“So the next task is to find a subset of genes that perform core processes for the parasites, but which are not shared with the human host,” says El-Sayed.
El-Sayed’s research has given insight into the “lifestyles” of the parasites. The one that causes sleeping sickness, Trypansosoma brucei, travels the bloodstream of its host and has more aliases than a top-secret spy, constantly reinventing itself to avoid detection by the immune system.
“It hides behind the smokescreen of 10 million molecules on its surface,” says Matthew Berriman, project leader at the Welcome Trust Sanger Institute in Hinxton, Cambridge.
This particular brand of parasite is 16 times as complex as the parasite that causes malaria, holding 800 genes constantly reshuffling to produce a chameleon-like presence.
Spread by the tsetse fly, T. Brucei causes sleeping sickness throughout equatorial Africa affecting 300,000 to 500,000 people yearly. It is fatal if untreated or if not treated early enough.
While the clever T. Brucei is a master of disguise, the other two parasites survive as stowaways inside human cells, feasting on amino acids and other building blocks.
Trypanosoma cruzi causes Chagas disease, which affects 18 million people and kills 45,000 a year. Spread by bloodsucking triatomine bugs, it has special genes that allow it to process histidine, an amino acid. T. cruzi is so effective at hiding inside the cell that it usually goes undetected until heart failure kills its host.
Leishmania major is the parasite spread by sand flies that causes leishmaniasis, a disfiguring disease that afflicts 12 million people in Latin America and the Middle East. Annual deaths are in the tens of thousands.
While these are very serious diseases affecting millions in the poorest of countries, little funding has been given to take scientists from gene-mapping to drug-making. The Bill and Melinda Gates foundation recently secured $450 million to tackle disease in developing nations, and many hope the G8 Summit will find more funding for the cause.
There are existing treatments for the diseases, but they are considered very toxic and risky. Melarsoprol, the most used drug against sleeping sickness is cut with arsenic, and then followed by an antidote. The treatment kills about five percent of recipients.
