SARS was first identified in China in 2003 and spread rapidly to Asia, Canada and elsewhere. It killed nearly 800 people and disrupted travel, economics and even some scientific meetings.

Learning how SARS (severe acute respiratory syndrome) became a deadly threat "possibly teaches us a lesson on how to actively fight so diverse and dreadful diseases as SARS, avian flu or the effects of such biotech weapons as anthrax," said Dr. Josef Penninger of the Institute of Molecular Biotechnology of the Austrian Academy of Sciences.

The research may have wider implications for a type of lung failure known as acute respiratory distress syndrome, Penninger reported in a communication to the journal Nature. It can occur in cases such as sepsis, aspiration of gastric contents, pneumonia and both avian and human influenza.

What those diseases have in common is a type of lung failure.

May Help Millions

Penninger and colleagues report in Monday's issue of Nature Medicine that, working in mice, they found that angiotensin-converting enzyme 2 (ACE2) is a crucial receptor for the SARS virus.

The result is disruption of the body's protective renin-angiotensin system, leading to respiratory distress syndrome as fluids seep into the air sacks. The renin-angiotensin system uses enzymes to regulate sodium balance, fluid volume and blood pressure.

SARS was first identified in 2003, originating in China and spreading rapidly to Asia, Canada and elsewhere. It killed nearly 800 people and disrupted travel, economics and even some scientific meetings.

The researchers found that the SARS virus binds to the ACE2, Penninger said in a telephone interview.

If disabling ACE2 allowed lung damage to occur, the researchers wondered whether providing more of the enzyme would help. They created more ACE2 and infused it into the mice. The result was to protect mice from the lung failure effects of SARS.

It was effective in two ways, Penninger said.

First, ACE2 combined with the virus and prevented it from binding to normal cells. Also, the enzyme protected the mice from acute lung failure.

"We of course need to extend these findings in mice now to humans," Penninger said. "Yet in essence, SARS pointed us to a protein that may help millions of people affected with a previously untreatable disease."

Productive Field for Investigation

A commentary by John Nicholls and Malik Peiris of the University of Hong Kong said the findings indicate that the potential therapeutic value of ACE2 and angiotensin 2 receptor inhibitors for acute lung injury will be a productive field for investigation.

But Peiris and Nicholls, who were not part of Penninger's team, said there are differences in the way SARS binds with human ACE2 and ACE2 in mice.

The research was funded by the Austrian Academy of Sciences, Austrian National Bank, Marie Curie Fellowship of the European Union, Beijing Committee of Science and Technology, National Natural Science Foundation of China, Joincare Corporation, Canadian Institutes of Health Research, Canada Foundation for Innovation and the German Research Council.