• Wenhui Li, Thomas C Greenough, Michael J Moore, Natalya Vasilieva, Mohan Somasundaran, John L Sullivan, Michael Farzan, and Hyeryun Choe.
• Partners AIDS Research Center, 65 Landsdowne St., Cambridge, MA 02139, USA.
• J. Virol. 2004 Oct 1; 78 (20): 11429-33.

AbstractReplication of viruses in species other than their natural hosts is frequently limited by entry and postentry barriers. The coronavirus that causes severe acute respiratory syndrome (SARS-CoV) utilizes the receptor angiotensin-converting enzyme 2 (ACE2) to infect cells. Here we compare human, mouse, and rat ACE2 molecules for their ability to serve as receptors for SARS-CoV. We found that, compared to human ACE2, murine ACE2 less efficiently bound the S1 domain of SARS-CoV and supported less-efficient S protein-mediated infection. Rat ACE2 was even less efficient, at near background levels for both activities. Murine 3T3 cells expressing human ACE2 supported SARS-CoV replication, whereas replication was less than 10% as efficient in the same cells expressing murine ACE2. These data imply that a mouse transgenically expressing human ACE2 may be a useful animal model of SARS.

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