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Joan Stephenson, PhD

JAMA. 2005;294:787.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

When severe acute respiratory syndrome (SARS) surfaced in 2003, the molecular mechanism underlying the SARS coronavirus’ ability to cause often lethal severe acute lung failure was a mystery. Now, researchers from Austria, China, the United States, and Canada have discovered a clue to how the SARS virus damages the lungs.

Previous studies in cultured cells had identified a protein known for its role in regulating blood pressure, angiotensin-converting enzyme 2 (ACE2), as a potential receptor for the SARS coronavirus. In the new work, reported on July 10 in the online edition of Nature Medicine (http://www.nature.com/nm/index.html), researchers demonstrated in mice that ACE2 is a crucial receptor for the virus in vivo. They found that when the Spike protein of the SARS virus binds to ACE2, it reduces ACE2 expression and blood vessels in the lungs leak fluid and damage the tissue.

Similar damage is found in . . . [Full Text of this Article]