SrasV1, PubMed, Corpus, bibRecord, 002B35

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

Identifieur interne : 002B35 ( PubMed/Corpus ); précédent : 002B34; suivant : 002B36

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

Auteurs : Wenhui Li ; Thomas C. Greenough ; Michael J. Moore ; Natalya Vasilieva ; Mohan Somasundaran ; John L. Sullivan ; Michael Farzan ; Hyeryun Choe

Source :

Journal of virology [ 0022-538X ] ; 2004.

RBID : pubmed:15452268

English descriptors

KwdEn :
- 3T3 Cells, Animals, Cell Line, Endopeptidases (metabolism), Humans, Mice, Peptidyl-Dipeptidase A (metabolism), Rats, SARS Virus (pathogenicity), SARS Virus (physiology), Severe Acute Respiratory Syndrome (virology), Virus Replication.
MESH :
- chemical , metabolism : Endopeptidases, Peptidyl-Dipeptidase A.
- pathogenicity : SARS Virus.
- physiology : SARS Virus.
- virology : Severe Acute Respiratory Syndrome.
- 3T3 Cells, Animals, Cell Line, Humans, Mice, Rats, Virus Replication.

Abstract

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.

DOI: 10.1128/JVI.78.20.11429-11433.2004
PubMed: 15452268

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pubmed:15452268

Le document en format XML

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<author><name sortKey="Li, Wenhui" sort="Li, Wenhui" uniqKey="Li W" first="Wenhui" last="Li">Wenhui Li</name>
<affiliation><nlm:affiliation>Partners AIDS Research Center, 65 Landsdowne St., Cambridge, MA 02139, USA.</nlm:affiliation>
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<author><name sortKey="Greenough, Thomas C" sort="Greenough, Thomas C" uniqKey="Greenough T" first="Thomas C" last="Greenough">Thomas C. Greenough</name>
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<author><name sortKey="Moore, Michael J" sort="Moore, Michael J" uniqKey="Moore M" first="Michael J" last="Moore">Michael J. Moore</name>
</author>
<author><name sortKey="Vasilieva, Natalya" sort="Vasilieva, Natalya" uniqKey="Vasilieva N" first="Natalya" last="Vasilieva">Natalya Vasilieva</name>
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<author><name sortKey="Somasundaran, Mohan" sort="Somasundaran, Mohan" uniqKey="Somasundaran M" first="Mohan" last="Somasundaran">Mohan Somasundaran</name>
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<author><name sortKey="Sullivan, John L" sort="Sullivan, John L" uniqKey="Sullivan J" first="John L" last="Sullivan">John L. Sullivan</name>
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<author><name sortKey="Farzan, Michael" sort="Farzan, Michael" uniqKey="Farzan M" first="Michael" last="Farzan">Michael Farzan</name>
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<author><name sortKey="Choe, Hyeryun" sort="Choe, Hyeryun" uniqKey="Choe H" first="Hyeryun" last="Choe">Hyeryun Choe</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Efficient replication of severe acute respiratory syndrome coronavirus in mouse cells is limited by murine angiotensin-converting enzyme 2.</title>
<author><name sortKey="Li, Wenhui" sort="Li, Wenhui" uniqKey="Li W" first="Wenhui" last="Li">Wenhui Li</name>
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<author><name sortKey="Vasilieva, Natalya" sort="Vasilieva, Natalya" uniqKey="Vasilieva N" first="Natalya" last="Vasilieva">Natalya Vasilieva</name>
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<term>Humans</term>
<term>Mice</term>
<term>Peptidyl-Dipeptidase A (metabolism)</term>
<term>Rats</term>
<term>SARS Virus (pathogenicity)</term>
<term>SARS Virus (physiology)</term>
<term>Severe Acute Respiratory Syndrome (virology)</term>
<term>Virus Replication</term>
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<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Endopeptidases</term>
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<keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>SARS Virus</term>
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<front><div type="abstract" xml:lang="en">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.</div>
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<Abstract><AbstractText>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.</AbstractText>
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Efficient replication of severe acute respiratory syndrome coronavirus in mouse cells is limited by murine angiotensin-converting enzyme 2.

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

Source :

English descriptors

Abstract

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Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

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