SrasV1, PascalFrancis, Corpus, bibRecord, 000639

Apical entry and release of severe acute respiratory syndrome-associated coronavirus in polarized calu-3 lung epithelial cells

Identifieur interne : 000639 ( PascalFrancis/Corpus ); précédent : 000638; suivant : 000640

Apical entry and release of severe acute respiratory syndrome-associated coronavirus in polarized calu-3 lung epithelial cells

Auteurs : Chien-Te K. Tseng ; Jennifer Tseng ; Lucy Perrone ; Melissa Worthy ; Vsevolod Popov ; Clarence J. Peters

Source :

Journal of virology [ 0022-538X ] ; 2005.

RBID : Pascal:05-0333831

Descripteurs français

Pascal (Inist)
- Coronavirus, Libération, Cellule épithéliale, Microbiologie, Virologie, Syndrome respiratoire aigu sévère.

English descriptors

KwdEn :
- Coronavirus, Epithelial cell, Microbiology, Release, Severe acute respiratory syndrome, Virology.

Abstract

Severe acute respiratory syndrome (SARS), caused by a novel coronavirus (CoV) known as SARS-CoV, is a contagious and life-threatening respiratory illness with pneumocytes as its main target. A full understanding of how SARS-CoV would interact with lung epithelial cells will be vital for advancing our knowledge of SARS pathogenesis. However, an in vitro model of SARS-CoV infection using relevant lung epithelial cells is not yet available, making it difficult to dissect the pathogenesis of SARS-CoV in the lungs. Here, we report that SARS-CoV can productively infect human bronchial epithelial Calu-3 cells, causing cytopathic effects, a process reflective of its natural course of infection in the lungs. Indirect immunofluorescence studies revealed a preferential expression of angiotensin-converting enzyme 2 (ACE-2), the functional receptor of SARS-CoV, on the apical surface. Importantly, both ACE-2 and viral antigen appeared to preferentially colocalize at the apical domain of infected cells. In highly polarized Calu-3 cells grown on the membrane inserts, we found that cells exposed to virus through the apical rather than the basolateral surface showed high levels of viral replication. Progeny virus was released into the apical chamber at titers up to 5 logs higher than those recovered from the basolateral chambers of polarized cultures. Taken together, these results indicate that SARS-CoV almost exclusively entered and was released from the apical domain of polarized Calu-3 cells, which might provide important insight into the mechanism of transmission and pathogenesis of SARS-CoV.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A11	`01`	`1`		`@1 TSENG (Chien-Te K.)`
A11	`02`	`1`		`@1 TSENG (Jennifer)`
A11	`03`	`1`		`@1 PERRONE (Lucy)`
A11	`04`	`1`		`@1 WORTHY (Melissa)`
A11	`05`	`1`		`@1 POPOV (Vsevolod)`
A11	`06`	`1`		`@1 PETERS (Clarence J.)`
A14	`01`			`@1 Department of Microbiology and Immunology, University of Texas Medical Branch @2 Galveston, Texas 77555-0609 @3 USA @Z 1 aut. @Z 4 aut. @Z 6 aut.`
A14	`02`			`@1 Department of Pathology, University of Texas Medical Branch @2 Galveston, Texas 77555-0609 @3 USA @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 5 aut. @Z 6 aut.`
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C01	`01`		`ENG`	@0 Severe acute respiratory syndrome (SARS), caused by a novel coronavirus (CoV) known as SARS-CoV, is a contagious and life-threatening respiratory illness with pneumocytes as its main target. A full understanding of how SARS-CoV would interact with lung epithelial cells will be vital for advancing our knowledge of SARS pathogenesis. However, an in vitro model of SARS-CoV infection using relevant lung epithelial cells is not yet available, making it difficult to dissect the pathogenesis of SARS-CoV in the lungs. Here, we report that SARS-CoV can productively infect human bronchial epithelial Calu-3 cells, causing cytopathic effects, a process reflective of its natural course of infection in the lungs. Indirect immunofluorescence studies revealed a preferential expression of angiotensin-converting enzyme 2 (ACE-2), the functional receptor of SARS-CoV, on the apical surface. Importantly, both ACE-2 and viral antigen appeared to preferentially colocalize at the apical domain of infected cells. In highly polarized Calu-3 cells grown on the membrane inserts, we found that cells exposed to virus through the apical rather than the basolateral surface showed high levels of viral replication. Progeny virus was released into the apical chamber at titers up to 5 logs higher than those recovered from the basolateral chambers of polarized cultures. Taken together, these results indicate that SARS-CoV almost exclusively entered and was released from the apical domain of polarized Calu-3 cells, which might provide important insight into the mechanism of transmission and pathogenesis of SARS-CoV.
C02	`01`	`X`		`@0 002A05C10`
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C03	`01`	`X`	`ENG`	`@0 Coronavirus @2 NW @5 01`
C03	`01`	`X`	`SPA`	`@0 Coronavirus @2 NW @5 01`
C03	`02`	`X`	`FRE`	`@0 Libération @5 05`
C03	`02`	`X`	`ENG`	`@0 Release @5 05`
C03	`02`	`X`	`SPA`	`@0 Liberación @5 05`
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C03	`04`	`X`	`ENG`	`@0 Microbiology @5 07`
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C03	`05`	`X`	`FRE`	`@0 Virologie @5 08`
C03	`05`	`X`	`ENG`	`@0 Virology @5 08`
C03	`05`	`X`	`SPA`	`@0 Virología @5 08`
C03	`06`	`X`	`FRE`	`@0 Syndrome respiratoire aigu sévère @2 NM @5 14`
C03	`06`	`X`	`ENG`	`@0 Severe acute respiratory syndrome @2 NM @5 14`
C03	`06`	`X`	`SPA`	`@0 Síndrome respiratorio agudo severo @2 NM @5 14`
C07	`01`	`X`	`FRE`	`@0 Coronaviridae @2 NW`
C07	`01`	`X`	`ENG`	`@0 Coronaviridae @2 NW`
C07	`01`	`X`	`SPA`	`@0 Coronaviridae @2 NW`
C07	`02`	`X`	`FRE`	`@0 Nidovirales @2 NW`
C07	`02`	`X`	`ENG`	`@0 Nidovirales @2 NW`
C07	`02`	`X`	`SPA`	`@0 Nidovirales @2 NW`
C07	`03`	`X`	`FRE`	`@0 Virus @2 NW`
C07	`03`	`X`	`ENG`	`@0 Virus @2 NW`
C07	`03`	`X`	`SPA`	`@0 Virus @2 NW`
C07	`04`	`X`	`FRE`	`@0 Poumon pathologie @5 13`
C07	`04`	`X`	`ENG`	`@0 Lung disease @5 13`
C07	`04`	`X`	`SPA`	`@0 Pulmón patología @5 13`
C07	`05`	`X`	`FRE`	`@0 Virose`
C07	`05`	`X`	`ENG`	`@0 Viral disease`
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N44	`01`			`@1 OTO`
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Format Inist (serveur)

NO :	PASCAL 05-0333831 INIST
ET :	Apical entry and release of severe acute respiratory syndrome-associated coronavirus in polarized calu-3 lung epithelial cells
AU :	TSENG (Chien-Te K.); TSENG (Jennifer); PERRONE (Lucy); WORTHY (Melissa); POPOV (Vsevolod); PETERS (Clarence J.)
AF :	Department of Microbiology and Immunology, University of Texas Medical Branch/Galveston, Texas 77555-0609/Etats-Unis (1 aut., 4 aut., 6 aut.); Department of Pathology, University of Texas Medical Branch/Galveston, Texas 77555-0609/Etats-Unis (1 aut., 2 aut., 3 aut., 5 aut., 6 aut.)
DT :	Publication en série; Niveau analytique
SO :	Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2005; Vol. 79; No. 15; Pp. 9470-9479; Bibl. 35 ref.
LA :	Anglais
EA :	Severe acute respiratory syndrome (SARS), caused by a novel coronavirus (CoV) known as SARS-CoV, is a contagious and life-threatening respiratory illness with pneumocytes as its main target. A full understanding of how SARS-CoV would interact with lung epithelial cells will be vital for advancing our knowledge of SARS pathogenesis. However, an in vitro model of SARS-CoV infection using relevant lung epithelial cells is not yet available, making it difficult to dissect the pathogenesis of SARS-CoV in the lungs. Here, we report that SARS-CoV can productively infect human bronchial epithelial Calu-3 cells, causing cytopathic effects, a process reflective of its natural course of infection in the lungs. Indirect immunofluorescence studies revealed a preferential expression of angiotensin-converting enzyme 2 (ACE-2), the functional receptor of SARS-CoV, on the apical surface. Importantly, both ACE-2 and viral antigen appeared to preferentially colocalize at the apical domain of infected cells. In highly polarized Calu-3 cells grown on the membrane inserts, we found that cells exposed to virus through the apical rather than the basolateral surface showed high levels of viral replication. Progeny virus was released into the apical chamber at titers up to 5 logs higher than those recovered from the basolateral chambers of polarized cultures. Taken together, these results indicate that SARS-CoV almost exclusively entered and was released from the apical domain of polarized Calu-3 cells, which might provide important insight into the mechanism of transmission and pathogenesis of SARS-CoV.
CC :	002A05C10
FD :	Coronavirus; Libération; Cellule épithéliale; Microbiologie; Virologie; Syndrome respiratoire aigu sévère
FG :	Coronaviridae; Nidovirales; Virus; Poumon pathologie; Virose; Infection; Appareil respiratoire pathologie
ED :	Coronavirus; Release; Epithelial cell; Microbiology; Virology; Severe acute respiratory syndrome
EG :	Coronaviridae; Nidovirales; Virus; Lung disease; Viral disease; Infection; Respiratory disease
SD :	Coronavirus; Liberación; Célula epitelial; Microbiología; Virología; Síndrome respiratorio agudo severo
LO :	INIST-13592.354000138598310110
ID :	05-0333831

Links to Exploration step

Pascal:05-0333831

Le document en format XML

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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Apical entry and release of severe acute respiratory syndrome-associated coronavirus in polarized calu-3 lung epithelial cells</title>
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<front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome (SARS), caused by a novel coronavirus (CoV) known as SARS-CoV, is a contagious and life-threatening respiratory illness with pneumocytes as its main target. A full understanding of how SARS-CoV would interact with lung epithelial cells will be vital for advancing our knowledge of SARS pathogenesis. However, an in vitro model of SARS-CoV infection using relevant lung epithelial cells is not yet available, making it difficult to dissect the pathogenesis of SARS-CoV in the lungs. Here, we report that SARS-CoV can productively infect human bronchial epithelial Calu-3 cells, causing cytopathic effects, a process reflective of its natural course of infection in the lungs. Indirect immunofluorescence studies revealed a preferential expression of angiotensin-converting enzyme 2 (ACE-2), the functional receptor of SARS-CoV, on the apical surface. Importantly, both ACE-2 and viral antigen appeared to preferentially colocalize at the apical domain of infected cells. In highly polarized Calu-3 cells grown on the membrane inserts, we found that cells exposed to virus through the apical rather than the basolateral surface showed high levels of viral replication. Progeny virus was released into the apical chamber at titers up to 5 logs higher than those recovered from the basolateral chambers of polarized cultures. Taken together, these results indicate that SARS-CoV almost exclusively entered and was released from the apical domain of polarized Calu-3 cells, which might provide important insight into the mechanism of transmission and pathogenesis of SARS-CoV.</div>
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<server><NO>PASCAL 05-0333831 INIST</NO>
<ET>Apical entry and release of severe acute respiratory syndrome-associated coronavirus in polarized calu-3 lung epithelial cells</ET>
<AU>TSENG (Chien-Te K.); TSENG (Jennifer); PERRONE (Lucy); WORTHY (Melissa); POPOV (Vsevolod); PETERS (Clarence J.)</AU>
<AF>Department of Microbiology and Immunology, University of Texas Medical Branch/Galveston, Texas 77555-0609/Etats-Unis (1 aut., 4 aut., 6 aut.); Department of Pathology, University of Texas Medical Branch/Galveston, Texas 77555-0609/Etats-Unis (1 aut., 2 aut., 3 aut., 5 aut., 6 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2005; Vol. 79; No. 15; Pp. 9470-9479; Bibl. 35 ref.</SO>
<LA>Anglais</LA>
<EA>Severe acute respiratory syndrome (SARS), caused by a novel coronavirus (CoV) known as SARS-CoV, is a contagious and life-threatening respiratory illness with pneumocytes as its main target. A full understanding of how SARS-CoV would interact with lung epithelial cells will be vital for advancing our knowledge of SARS pathogenesis. However, an in vitro model of SARS-CoV infection using relevant lung epithelial cells is not yet available, making it difficult to dissect the pathogenesis of SARS-CoV in the lungs. Here, we report that SARS-CoV can productively infect human bronchial epithelial Calu-3 cells, causing cytopathic effects, a process reflective of its natural course of infection in the lungs. Indirect immunofluorescence studies revealed a preferential expression of angiotensin-converting enzyme 2 (ACE-2), the functional receptor of SARS-CoV, on the apical surface. Importantly, both ACE-2 and viral antigen appeared to preferentially colocalize at the apical domain of infected cells. In highly polarized Calu-3 cells grown on the membrane inserts, we found that cells exposed to virus through the apical rather than the basolateral surface showed high levels of viral replication. Progeny virus was released into the apical chamber at titers up to 5 logs higher than those recovered from the basolateral chambers of polarized cultures. Taken together, these results indicate that SARS-CoV almost exclusively entered and was released from the apical domain of polarized Calu-3 cells, which might provide important insight into the mechanism of transmission and pathogenesis of SARS-CoV.</EA>
<CC>002A05C10</CC>
<FD>Coronavirus; Libération; Cellule épithéliale; Microbiologie; Virologie; Syndrome respiratoire aigu sévère</FD>
<FG>Coronaviridae; Nidovirales; Virus; Poumon pathologie; Virose; Infection; Appareil respiratoire pathologie</FG>
<ED>Coronavirus; Release; Epithelial cell; Microbiology; Virology; Severe acute respiratory syndrome</ED>
<EG>Coronaviridae; Nidovirales; Virus; Lung disease; Viral disease; Infection; Respiratory disease</EG>
<SD>Coronavirus; Liberación; Célula epitelial; Microbiología; Virología; Síndrome respiratorio agudo severo</SD>
<LO>INIST-13592.354000138598310110</LO>
<ID>05-0333831</ID>
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Apical entry and release of severe acute respiratory syndrome-associated coronavirus in polarized calu-3 lung epithelial cells

Apical entry and release of severe acute respiratory syndrome-associated coronavirus in polarized calu-3 lung epithelial cells

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