Efficient replication of severe acute respiratory syndrome coronavirus in mouse cells is limited by murine angiotensin-converting enzyme 2

被引:122
|
作者
Li, WH
Greenough, TC
Moore, MJ
Vasilieva, N
Somasundaran, M
Sullivan, JL
Farzan, M
Choe, H
机构
[1] Harvard Univ, Sch Med, Brigham & Womens Hosp,Partners AIDS Res Ctr, Dept Med Microbiol & Mol Genet, Boston, MA 02115 USA
[2] Harvard Univ, Sch Med, Childrens Hosp, Dept Med,Pulm Div, Boston, MA 02115 USA
[3] Univ Massachusetts, Sch Med, Program Mol Med, Worcester, MA 01605 USA
关键词
D O I
10.1128/JVI.78.20.11429-11433.2004
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Replication 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.
引用
收藏
页码:11429 / 11433
页数:5
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