Previous epidemic-causing viruses have mutated and died out naturally. Credit: © Corbis

The SARS virus may be with us for some time to come. Its genetic makeup is showing little sign of change, say researchers. But this may make the spread of the killer easier to track, and could buy scientists more time to produce an effective vaccine.

It also means that the virus is unlikely to mutate into a benign form as did previous epidemic-causing ones, explains virologist Earl Brown of the University of Ottawa, Canada. A lethal strain of SIV, an HIV-like virus that affected chimps, has disappeared this way.

However, the SARS virus only appeared in November 2002, so "it may be too early to draw general conclusions", says Albert Osterhaus, who is working on the infectivity of the virus at Erasmus University in Rotterdam, the Netherlands.

The infective agent behind SARS - the respiratory condition that has to date infected more than 7,000 and killed over 500 - is thought to be a new coronavirus. Normally, coronavirus genomes are highly labile.

Tracking a killer

Edison Liu and his colleagues at the Genome Institute of Singapore cultured and compared SARS virus samples taken from Singapore, Canada, Hong Kong, and Guangzhou and Beijing in China. They found that the majority of the virus genome has remained unchanged as the infection has spread.

The handful of genetic modifications that have occurred as the virus has spread from place to place over the past five months may help to trace the origin of infection. SARS viruses from different countries can have subtly different "molecular signatures", says Liu.

It may be too early to draw general conclusions Albert Osterhaus , Erasmus University

Some of these changes may have occurred in the laboratory, warns Osterhaus. Before the virus was analysed, it was grown in monkey cells. The mutations may have arisen as the virus adapted to its new host. He suggests that virus taken from or cultured in human cells should be studied instead.

"There is a great need now for genetic analysis of a less serious virus," says virologist John Oxford from the London Queen Mary's School of Medicine. He suggests that researchers isolate and sequence virus from patients with only minor symptoms. These data could be compared against those from lethal strains, to pinpoint the genes that turn a virus into a killer. These would offer new targets for drug and vaccine development.