SrasV1, Main, Exploration, bibRecord, 005B41

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

Identifieur interne : 005B41 ( Main/Exploration ); précédent : 005B40; suivant : 005B42

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

Auteurs : WENHUI LI [États-Unis] ; Thomas C. Greenough [États-Unis] ; Michael J. Moore [États-Unis] ; Natalya Vasilieva [États-Unis] ; Mohan Somasundaran [États-Unis] ; John L. Sullivan [États-Unis] ; Michael Farzan [États-Unis] ; Hyeryun Choe [États-Unis]

Source :

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

RBID : Pascal:04-0554589

Descripteurs français

Pascal (Inist)
- Coronavirus, Souris, Réplication, Grave, Malade état grave, Aigu, Voie respiratoire, Animal, Angiotensine, Peptidyl-dipeptidase A, Syndrome respiratoire aigu sévère, Microbiologie, Virologie, Forme grave.

English descriptors

KwdEn :
- Acute, Angiotensin, Animal, Coronavirus, Critically ill, Microbiology, Mouse, Peptidyl-dipeptidase A, Replication, Respiratory tract, Severe, Severe acute respiratory syndrome, Virology.

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.

Affiliations:

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Le document en format XML

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<term>Peptidyl-dipeptidase A</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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<name sortKey="Vasilieva, Natalya" sort="Vasilieva, Natalya" uniqKey="Vasilieva N" first="Natalya" last="Vasilieva">Natalya Vasilieva</name>
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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 :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri