Shanghai

Geneticists are taking some early steps towards a fresh strategy to combat 'snail fever', a potentially fatal liver disease that affects more than a million people in China.

A team led by scientists at the Chinese National Human Genome Center in Shanghai this week published details of some 13,000 genes of the parasitic worm Schistosoma japonicum that causes the condition (W. Hu et al. Nature Genet. doi:10.1038/ng1236). Researchers now hope that an analysis of the parasite's genome will help to combat its spread.

The worm lives in freshwater snails found chiefly along the Yangtze river in central China. According to Chinese researchers, snail fever, or schistosomiasis, was fairly prevalent until the 1950s, when rudimentary public-health measures helped to curb its spread. But it has recently been making a comeback, and in July Chinese vice-premier Yi Wu ranked it next to severe acute respiratory syndrome (SARS) and AIDS as one of China's main public-health challenges.

Other species of the worm, most notably S. mansoni, infect humans, mainly in South America and Africa. The World Health Organization estimates that up to 200 million people in more than 70 countries are infected with Schistosoma.

The worm passes from its host into fresh water, from where it can penetrate human skin and infect various organs. About 40 days after entering the body, it produces eggs in the liver that can block blood flow there. Symptoms include fever, stiffness of limbs and an enlarged liver and spleen. Up to 65 million people living in tropical areas of China are at risk of contracting the potentially fatal disease, public-health officials say.

Almost 50 years ago, China's government mobilized tens of thousands of peasants to take steps to reduce the number of people infected, including collecting and burying snails in soil. But recently the number of cases has increased again. The World Health Organization has cited construction of the Three Gorges Dam on the Yangtze as a possible factor in the disease's revival.

Schistosomiasis can be treated with various drugs, but these are expensive and do not prevent reinfection. Health officials are also concerned that the worm may become resistant to drug treatment.

Ze-Guang Han, the geneticist who led the latest study, says that his team has identified several candidate genes encoding proteins that are specific to the worm and that could be used as the basis for a vaccine to immunize people against the disease. They include proteins found on the parasite's cell membrane and those involved in egg generation. “The development of a vaccine is critical for many developing countries,” Han says.

According to the researchers, their work also offers some insight into the worm's unusual life cycle. Early on, for example, the male and female parasites are separate entities, but as adults the female lives tucked inside the male. “Biologically, this is a unique organism for study,” says Guo-Ping Zhao, the Shanghai centre's deputy director.

The study shows that many receptor proteins on the surface of worm cells, which respond to signalling molecules from other cells, are similar to those found in the worm's various hosts. This partly explains how the worm hijacks its host's signals to spur its own proliferation and how it evades detection by the host's immune system. “We can really understand the interplay between the host and parasite,” says Han.

The Shanghai centre now plans to sequence the parasite's entire genome, which is estimated to contain up to 270 million base pairs. Researchers in the United States are already leading an international effort to sequence the genome of S. mansoni.