A paper in the August issue of Nature Medicine reports that angiotensin-converting enzyme 2 (ACE2) is a crucial receptor of the severe acute respiratory syndrome (SARS) virus in vivo.
In 2003, a new pathogen-the SARS virus-spread rapidly through the world, causing severe pneumonia and lethal lung failure. In cell lines, ACE2, a protein well known for its role in regulating blood pressure, had been identified as a potential SARS receptor. Now, Josef Penninger and colleagues provide the first genetic proof that ACE2 is the SARS receptor in vivo.
They found that SARS infections and the Spike protein of the SARS virus reduce ACE2 expression, leading to leak from lung blood vessels and subsequent damage. Injection of the Spike protein into mice worsens acute lung failure in vivo, an effect that can be attenuated by blocking the renin-angiotensin pathway, through which ACE2 normally works.
The findings of Penninger and colleagues provide a molecular explanation for why SARS infections cause severe lung failure and suggest a rational therapy for SARS and possibly other respiratory disease viruses. In fact, a paper from the same group published in the 7 July issue of Nature (436. pp111-115) shows that ACE2 can also protect mice from severe acute lung failure induced by acute respiratory distress syndrome (ARDS).
A related News and Views article by John Nicholls and Malik Peiris, placing the findings in a broader context, will accompany this article.
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