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Retroviruses pseudotyped with the severe acute respiratory syndrome coronavirus spike protein efficiently infect cells expressing angiotensin-converting enzyme 2

Identifieur interne : 005A74 ( Main/Exploration ); précédent : 005A73; suivant : 005A75

Retroviruses pseudotyped with the severe acute respiratory syndrome coronavirus spike protein efficiently infect cells expressing angiotensin-converting enzyme 2

Auteurs : Michael J. Moore [États-Unis] ; Tatyana Dorfman [États-Unis] ; WENHUI LI [États-Unis] ; SWEE KEE WONG [États-Unis] ; YANHAN LI [République populaire de Chine] ; Jens H. Kuhn [États-Unis, Allemagne] ; James Coderre [États-Unis] ; Natalya Vasilieva [États-Unis] ; ZHONGCHAO HAN [République populaire de Chine] ; Thomas C. Greenough [États-Unis] ; Michael Farzan [États-Unis] ; HYERYUN CHOE [États-Unis]

Source :

RBID : Pascal:04-0527890

Descripteurs français

English descriptors

Abstract

Infection of receptor-bearing cells by coronaviruses is mediated by their spike (S) proteins. The coronavirus (SARS-CoV) that causes severe acute respiratory syndrome (SARS) infects cells expressing the receptor angiotensin-converting enzyme 2 (ACE2). Here we show that codon optimization of the SARS-CoV S-protein gene substantially enhanced S-protein expression. We also found that two retroviruses, simian immunodeficiency virus (SIV) and murine leukemia virus, both expressing green fluorescent protein and pseudotyped with SARS-CoV S protein or S-protein variants, efficiently infected HEK293T cells stably expressing ACE2. Infection mediated by an S-protein variant whose cytoplasmic domain had been truncated and altered to include a fragment of the cytoplasmic tail of the human immunodeficiency virus type 1 envelope glycoprotein was, in both cases, substantially more efficient than that mediated by wild-type S protein. Using S-protein-pseudotyped SIV, we found that the enzymatic activity of ACE2 made no contribution to S-protein-mediated infection. Finally, we show that a soluble and catalytically inactive form of ACE2 potently blocked infection by S-protein-pseudotyped retrovirus and by SARS-CoV. These results permit studies of SARS-CoV entry inhibitors without the use of live virus and suggest a candidate therapy for SARS.


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<title level="j" type="main">Journal of virology</title>
<title level="j" type="abbreviated">J. virol.</title>
<idno type="ISSN">0022-538X</idno>
</seriesStmt>
</fileDesc>
<profileDesc>
<textClass>
<keywords scheme="KwdEn" xml:lang="en">
<term>Acute</term>
<term>Amino Acid Sequence</term>
<term>Angiotensin</term>
<term>Animals</term>
<term>Carboxypeptidases (genetics)</term>
<term>Carboxypeptidases (metabolism)</term>
<term>Cell Line</term>
<term>Coronavirus</term>
<term>Critically ill</term>
<term>HIV-1 (genetics)</term>
<term>Humans</term>
<term>Infected cell</term>
<term>Leukemia Virus, Murine (genetics)</term>
<term>Leukemia Virus, Murine (metabolism)</term>
<term>Leukemia Virus, Murine (physiology)</term>
<term>Membrane Glycoproteins (genetics)</term>
<term>Membrane Glycoproteins (metabolism)</term>
<term>Microbiology</term>
<term>Molecular Sequence Data</term>
<term>Peptidyl-Dipeptidase A</term>
<term>Peptidyl-dipeptidase A</term>
<term>Protein</term>
<term>Receptors, Virus (metabolism)</term>
<term>Respiratory tract</term>
<term>Retroviridae</term>
<term>SARS Virus (genetics)</term>
<term>Severe</term>
<term>Severe acute respiratory syndrome</term>
<term>Simian Immunodeficiency Virus (genetics)</term>
<term>Simian Immunodeficiency Virus (metabolism)</term>
<term>Simian Immunodeficiency Virus (physiology)</term>
<term>Spike Glycoprotein, Coronavirus</term>
<term>Viral Envelope Proteins (genetics)</term>
<term>Viral Envelope Proteins (metabolism)</term>
<term>Virion (chemistry)</term>
<term>Virion (metabolism)</term>
<term>Virology</term>
<term>Virus Replication</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr">
<term>Animaux</term>
<term>Carboxypeptidases (génétique)</term>
<term>Carboxypeptidases (métabolisme)</term>
<term>Données de séquences moléculaires</term>
<term>Glycoprotéine de spicule des coronavirus</term>
<term>Glycoprotéines membranaires (génétique)</term>
<term>Glycoprotéines membranaires (métabolisme)</term>
<term>Humains</term>
<term>Lignée cellulaire</term>
<term>Peptidyl-Dipeptidase A</term>
<term>Protéines de l'enveloppe virale (génétique)</term>
<term>Protéines de l'enveloppe virale (métabolisme)</term>
<term>Récepteurs viraux (métabolisme)</term>
<term>Réplication virale</term>
<term>Séquence d'acides aminés</term>
<term>VIH-1 (Virus de l'Immunodéficience Humaine de type 1) (génétique)</term>
<term>Virion ()</term>
<term>Virion (métabolisme)</term>
<term>Virus de l'immunodéficience simienne (génétique)</term>
<term>Virus de l'immunodéficience simienne (métabolisme)</term>
<term>Virus de l'immunodéficience simienne (physiologie)</term>
<term>Virus de la leucémie murine (génétique)</term>
<term>Virus de la leucémie murine (métabolisme)</term>
<term>Virus de la leucémie murine (physiologie)</term>
<term>Virus du SRAS (génétique)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en">
<term>Carboxypeptidases</term>
<term>Membrane Glycoproteins</term>
<term>Viral Envelope Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en">
<term>Carboxypeptidases</term>
<term>Membrane Glycoproteins</term>
<term>Receptors, Virus</term>
<term>Viral Envelope Proteins</term>
</keywords>
<keywords scheme="MESH" qualifier="chemistry" xml:lang="en">
<term>Virion</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en">
<term>HIV-1</term>
<term>Leukemia Virus, Murine</term>
<term>SARS Virus</term>
<term>Simian Immunodeficiency Virus</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr">
<term>Carboxypeptidases</term>
<term>Glycoprotéines membranaires</term>
<term>Protéines de l'enveloppe virale</term>
<term>VIH-1 (Virus de l'Immunodéficience Humaine de type 1)</term>
<term>Virus de l'immunodéficience simienne</term>
<term>Virus de la leucémie murine</term>
<term>Virus du SRAS</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en">
<term>Leukemia Virus, Murine</term>
<term>Simian Immunodeficiency Virus</term>
<term>Virion</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr">
<term>Carboxypeptidases</term>
<term>Glycoprotéines membranaires</term>
<term>Protéines de l'enveloppe virale</term>
<term>Récepteurs viraux</term>
<term>Virion</term>
<term>Virus de l'immunodéficience simienne</term>
<term>Virus de la leucémie murine</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr">
<term>Virus de l'immunodéficience simienne</term>
<term>Virus de la leucémie murine</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en">
<term>Leukemia Virus, Murine</term>
<term>Simian Immunodeficiency Virus</term>
</keywords>
<keywords scheme="MESH" xml:lang="en">
<term>Amino Acid Sequence</term>
<term>Animals</term>
<term>Cell Line</term>
<term>Humans</term>
<term>Molecular Sequence Data</term>
<term>Peptidyl-Dipeptidase A</term>
<term>Spike Glycoprotein, Coronavirus</term>
<term>Virus Replication</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr">
<term>Animaux</term>
<term>Données de séquences moléculaires</term>
<term>Glycoprotéine de spicule des coronavirus</term>
<term>Humains</term>
<term>Lignée cellulaire</term>
<term>Peptidyl-Dipeptidase A</term>
<term>Retroviridae</term>
<term>Coronavirus</term>
<term>Grave</term>
<term>Malade état grave</term>
<term>Aigu</term>
<term>Réplication virale</term>
<term>Séquence d'acides aminés</term>
<term>Virion</term>
<term>Voie respiratoire</term>
<term>Protéine</term>
<term>Cellule infectée</term>
<term>Angiotensine</term>
<term>Peptidyl-dipeptidase A</term>
<term>Syndrome respiratoire aigu sévère</term>
<term>Microbiologie</term>
<term>Virologie</term>
<term>Forme grave</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front>
<div type="abstract" xml:lang="en">Infection of receptor-bearing cells by coronaviruses is mediated by their spike (S) proteins. The coronavirus (SARS-CoV) that causes severe acute respiratory syndrome (SARS) infects cells expressing the receptor angiotensin-converting enzyme 2 (ACE2). Here we show that codon optimization of the SARS-CoV S-protein gene substantially enhanced S-protein expression. We also found that two retroviruses, simian immunodeficiency virus (SIV) and murine leukemia virus, both expressing green fluorescent protein and pseudotyped with SARS-CoV S protein or S-protein variants, efficiently infected HEK293T cells stably expressing ACE2. Infection mediated by an S-protein variant whose cytoplasmic domain had been truncated and altered to include a fragment of the cytoplasmic tail of the human immunodeficiency virus type 1 envelope glycoprotein was, in both cases, substantially more efficient than that mediated by wild-type S protein. Using S-protein-pseudotyped SIV, we found that the enzymatic activity of ACE2 made no contribution to S-protein-mediated infection. Finally, we show that a soluble and catalytically inactive form of ACE2 potently blocked infection by S-protein-pseudotyped retrovirus and by SARS-CoV. These results permit studies of SARS-CoV entry inhibitors without the use of live virus and suggest a candidate therapy for SARS.</div>
</front>
</TEI>
<affiliations>
<list>
<country>
<li>Allemagne</li>
<li>République populaire de Chine</li>
<li>États-Unis</li>
</country>
<region>
<li>Berlin</li>
<li>Massachusetts</li>
</region>
<settlement>
<li>Berlin</li>
<li>Boston</li>
<li>Tianjin</li>
</settlement>
</list>
<tree>
<country name="États-Unis">
<region name="Massachusetts">
<name sortKey="Moore, Michael J" sort="Moore, Michael J" uniqKey="Moore M" first="Michael J." last="Moore">Michael J. Moore</name>
</region>
<name sortKey="Coderre, James" sort="Coderre, James" uniqKey="Coderre J" first="James" last="Coderre">James Coderre</name>
<name sortKey="Dorfman, Tatyana" sort="Dorfman, Tatyana" uniqKey="Dorfman T" first="Tatyana" last="Dorfman">Tatyana Dorfman</name>
<name sortKey="Farzan, Michael" sort="Farzan, Michael" uniqKey="Farzan M" first="Michael" last="Farzan">Michael Farzan</name>
<name sortKey="Greenough, Thomas C" sort="Greenough, Thomas C" uniqKey="Greenough T" first="Thomas C." last="Greenough">Thomas C. Greenough</name>
<name sortKey="Hyeryun Choe" sort="Hyeryun Choe" uniqKey="Hyeryun Choe" last="Hyeryun Choe">HYERYUN CHOE</name>
<name sortKey="Kuhn, Jens H" sort="Kuhn, Jens H" uniqKey="Kuhn J" first="Jens H." last="Kuhn">Jens H. Kuhn</name>
<name sortKey="Swee Kee Wong" sort="Swee Kee Wong" uniqKey="Swee Kee Wong" last="Swee Kee Wong">SWEE KEE WONG</name>
<name sortKey="Vasilieva, Natalya" sort="Vasilieva, Natalya" uniqKey="Vasilieva N" first="Natalya" last="Vasilieva">Natalya Vasilieva</name>
<name sortKey="Wenhui Li" sort="Wenhui Li" uniqKey="Wenhui Li" last="Wenhui Li">WENHUI LI</name>
</country>
<country name="République populaire de Chine">
<noRegion>
<name sortKey="Yanhan Li" sort="Yanhan Li" uniqKey="Yanhan Li" last="Yanhan Li">YANHAN LI</name>
</noRegion>
<name sortKey="Zhongchao Han" sort="Zhongchao Han" uniqKey="Zhongchao Han" last="Zhongchao Han">ZHONGCHAO HAN</name>
</country>
<country name="Allemagne">
<region name="Berlin">
<name sortKey="Kuhn, Jens H" sort="Kuhn, Jens H" uniqKey="Kuhn J" first="Jens H." last="Kuhn">Jens H. Kuhn</name>
</region>
</country>
</tree>
</affiliations>
</record>

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