Efficient replication of severe acute respiratory syndrome coronavirus in mouse cells is limited by murine angiotensin-converting enzyme 2
Greenough, Thomas C.
Moore, Michael J.
Sullivan, John L.
UMass Chan AffiliationsProgram in Molecular Medicine
Department of Pediatrics
Document TypeJournal Article
Severe Acute Respiratory Syndrome
Immunology and Infectious Disease
MetadataShow full item record
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.
SourceJ Virol. 2004 Oct;78(20):11429-33. Link to article on publisher's site
Permanent Link to this Itemhttp://hdl.handle.net/20.500.14038/43459
Related ResourcesLink to Article in PubMed