Schistosomiasis genome could lead way to new treatments

Cracking the genetic code of an organism is key to understanding what makes an organism unique. In the case of a parasite like Shistosoma haematobium, the genome can tell us something about the tools an organism uses to gain access to our body, how it makes us sick or, most importantly, where we can find its weak spots. The genome, or complete DNA sequence, can thus help us find very specific weapons to fight disease. In a press statement released today, University of Melbourne researchers announced that they have cracked the schistosome genome, unleashing a wealth of information that can be used to identify new interventions to combat a disease that infects more than 112 people. You can read the full press release below or find it linked here.

Genetic code cracked for a devastating blood parasite

18 Jan 2012

Scientists have cracked the genetic code and predicted some high priority drug targets for the blood parasite Schistosoma haematobium, which is linked to bladder cancer and HIV/ AIDS and causes the insidious urogenital disease schistosomiasis haematobia in more than 112 million people in Africa.

Schistomiasis is recognised by the World Health Organization as one of the most socioeconomically devastating diseases, besides malaria, and is in urgent need of extensive research and improved control.

Dr Neil Young and Professor Robin Gasser from the University of Melbourne’s Faculty of Veterinary Science led the project conducted with the world’s largest genome sequencing facility, BGI-Shenzhen and an international research team. They sequenced the nuclear genome of Schistosoma haematobium from a single pair of tiny worms using an advanced approach. The work has been published in the latest issue of the journal Nature Genetics.

Schistosoma haematobium is one of three related species of schistosome to be sequenced, but is the most devastating, particularly because of its link to cancer and AIDS. The other two species are Schistosoma mansoni (Africa and South America) and Schistosoma japonicum (in parts of Asia) which both cause intestinal/liver disease in humans.

“This genome was the missing piece of a puzzle in schistosomiasis research. By revealing the genetic blueprint of Schistosoma haematobium, we now have a biological road map of the three major parasite species responsible for human schistosomiasis globally. Most importantly, the genome of Schistosoma haematobium will offer insights into how the intimate relationship between a parasite and its human host can induce malignant bladder cancer,” Dr Young said.

“Currently there is no vaccine and only one drug available to treat Schistosoma haematobium infection, so revealing its genetic blueprint provides an unprecedented resource for the design of new disease interventions, including drugs and vaccines.”

Schistosoma haematobium is transmitted from a freshwater snail to humans. Worms dwell in blood vessels and release eggs that become embedded in the bladder wall, and cause chronic immune-mediated disease and induce cancer.

The research was conducted in collaboration with BGI-Shenzhen, PR China; Instituto Nacional de Ciência e Tecnologia em Doenças Tropicais Instituto de Pesquisa René Rachou-Fiocruz, Belo Horizonte, Brasil; Griffith University, Brisbane, Queensland, Australia; James Cook University, Cairns, Queensland, Australia; Macquarie University, Sydney, New South Wales, Australia; National University of Singapore, Singapore; Natural History Museum, London, UK; Universidad de la República, Montevideo, Uruguay; George Washington University, Washington DC, USA.

The research was jointly funded by the Australian Research Council, BGI-Shenzhen and the National Health and Medical Research Council.

About Amy Alabaster

Amy is a communications intern for the Global Network and the Sabin Vaccine Institute. Before joining Sabin, Amy worked as a writer for the NIH Research Matters publication and as an NIH Fellow for the Laboratory of Malaria and Vector Research. She has an M.S. degree in biochemistry from the University of Arizona.

Leave a Reply