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.
Stephenson J. SARS Clue. JAMA. 2005;294(7):787. doi:10.1001/jama.294.7.787-a