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Severe acute respiratory syndrome (SARS) originated in southern China in November 2002, and soon spread to people on six continents, killing nearly 800 people all told. For the first time, researchers have identified a crucial SARS receptor in vivo that helps explain how and why SARS infection causes lung failure. The findings should help researchers treat other diseases that compromise lung function.
Previous research using cell lines had identified ACE2, a protein involved in regulating blood pressure, as a potential SARS receptor. Now Josef Penninger of the Institute of Molecular Biotechnology (IMBA) in Vienna, Austria, and his colleagues have tested the hypothesis in mice. In a paper published online yesterday by Nature Medicine, they report that SARS infection, and specifically the SARS protein known as Spike, reduces ACE2 expression. As a result, blood vessels in the lungs become damaged and the lung becomes flooded as a result.
In a second paper published in the current issue of the journal Nature, the same team of scientists reports that treating mice with ACE2 can protect the animals from lung failure brought on by another condition, acute respiratory distress syndrome (ARDS). "We of course need to extend these findings in mice now to humans," Penninger says. "Yet in essence, SARS pointed us to a protein that may help millions of people affected with a previously untreatable disease." Indeed, John Nicholls and Malik Peiris of the University of Hong Kong note in an accompanying commentary in Nature Medicine that the results could be applied to acute lung injuries arising from viruses and other causes, including a potential avian flu pandemic.
