SrasV1, PascalFrancis, Corpus, bibRecord, 000567

ACE2 receptor expression and severe acute respiratory syndrome coronavirus infection depend on differentiation of human airway epithelia

Identifieur interne : 000567 ( PascalFrancis/Corpus ); précédent : 000566; suivant : 000568

ACE2 receptor expression and severe acute respiratory syndrome coronavirus infection depend on differentiation of human airway epithelia

Auteurs : HONG PENG JIA ; Dwight C. Look ; LEI SHI ; Melissa Hickey ; Lecia Pewe ; Jason Netland ; Michael Farzan ; Christine Wohlford-Lenane ; Stanley Perlman ; Paul B. Jr Mccray

Source :

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

RBID : Pascal:06-0013780

Descripteurs français

Pascal (Inist)
- Coronavirus, Homme, Voie respiratoire, Microbiologie, Virologie, Syndrome respiratoire aigu sévère.

English descriptors

KwdEn :
- Coronavirus, Human, Microbiology, Respiratory tract, Severe acute respiratory syndrome, Virology.

Abstract

Studies of patients with severe acute respiratory syndrome (SARS) demonstrate that the respiratory tract is a major site of SARS-coronavirus (CoV) infection and disease morbidity. We studied host-pathogen interactions using native lung tissue and a model of well-differentiated cultures of primary human airway epithelia. Angiotensin converting enzyme 2 (ACE2), the receptor for both the SARS-CoV and the related human respiratory coronavirus NL63, was expressed in human airway epithelia as well as lung parenchyma. As assessed by immunofluorescence staining and membrane biotinylation, ACE2 protein was more abundantly expressed on the apical than the basolateral surface of polarized airway epithelia. Interestingly, ACE2 expression positively correlated with the differentiation state of epithelia. Undifferentiated cells expressing little ACE2 were poorly infected with SARS-CoV, while well-differentiated cells expressing more ACE2 were readily infected. Expression of ACE2 in poorly differentiated epithelia facilitated SARS spike (S) protein-pseudotyped virus entry. Consistent with the expression pattern of ACE2, the entry of SARS-CoV or a lentivirus pseudotyped with SARS-CoV S protein in differentiated epithelia was more efficient when applied to the apical surface. Furthermore, SARS-CoV replicated in polarized epithelia and preferentially exited via the apical surface. The results indicate that infection of human airway epithelia by SARS coronavirus correlates with the state of cell differentiation and ACE2 expression and localization. These findings have implications for understanding disease pathogenesis associated with SARS-CoV and NL63 infections.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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Format Inist (serveur)

NO :	PASCAL 06-0013780 INIST
ET :	ACE2 receptor expression and severe acute respiratory syndrome coronavirus infection depend on differentiation of human airway epithelia
AU :	HONG PENG JIA; LOOK (Dwight C.); LEI SHI; HICKEY (Melissa); PEWE (Lecia); NETLAND (Jason); FARZAN (Michael); WOHLFORD-LENANE (Christine); PERLMAN (Stanley); MCCRAY (Paul B. JR)
AF :	Department of Pediatrics, Carver College of Medicine, University of Iowa/Iowa City, Iowa 52242/Etats-Unis (1 aut., 4 aut., 5 aut., 6 aut., 8 aut., 9 aut., 10 aut.); Department of Internal Medicine, Carver College of Medicine, University of Iowa/Iowa City, Iowa 52242/Etats-Unis (2 aut., 3 aut.); Department of Microbiology and Molecular Genetics, Harvard University/Cambridge, Massachusetts 02138/Etats-Unis (7 aut.)
DT :	Publication en série; Niveau analytique
SO :	Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2005; Vol. 79; No. 23; Pp. 14614-14621; Bibl. 49 ref.
LA :	Anglais
EA :	Studies of patients with severe acute respiratory syndrome (SARS) demonstrate that the respiratory tract is a major site of SARS-coronavirus (CoV) infection and disease morbidity. We studied host-pathogen interactions using native lung tissue and a model of well-differentiated cultures of primary human airway epithelia. Angiotensin converting enzyme 2 (ACE2), the receptor for both the SARS-CoV and the related human respiratory coronavirus NL63, was expressed in human airway epithelia as well as lung parenchyma. As assessed by immunofluorescence staining and membrane biotinylation, ACE2 protein was more abundantly expressed on the apical than the basolateral surface of polarized airway epithelia. Interestingly, ACE2 expression positively correlated with the differentiation state of epithelia. Undifferentiated cells expressing little ACE2 were poorly infected with SARS-CoV, while well-differentiated cells expressing more ACE2 were readily infected. Expression of ACE2 in poorly differentiated epithelia facilitated SARS spike (S) protein-pseudotyped virus entry. Consistent with the expression pattern of ACE2, the entry of SARS-CoV or a lentivirus pseudotyped with SARS-CoV S protein in differentiated epithelia was more efficient when applied to the apical surface. Furthermore, SARS-CoV replicated in polarized epithelia and preferentially exited via the apical surface. The results indicate that infection of human airway epithelia by SARS coronavirus correlates with the state of cell differentiation and ACE2 expression and localization. These findings have implications for understanding disease pathogenesis associated with SARS-CoV and NL63 infections.
CC :	002A05C10
FD :	Coronavirus; Homme; Voie respiratoire; Microbiologie; Virologie; Syndrome respiratoire aigu sévère
FG :	Coronaviridae; Nidovirales; Virus; Appareil respiratoire pathologie; Virose; Infection; Poumon pathologie; Appareil respiratoire
ED :	Coronavirus; Human; Respiratory tract; Microbiology; Virology; Severe acute respiratory syndrome
EG :	Coronaviridae; Nidovirales; Virus; Respiratory disease; Viral disease; Infection; Lung disease; Respiratory system
SD :	Coronavirus; Hombre; Vía respiratoria; Microbiología; Virología; Síndrome respiratorio agudo severo
LO :	INIST-13592.354000135123560160
ID :	06-0013780

Links to Exploration step

Pascal:06-0013780

Le document en format XML

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<idno type="ISSN">0022-538X</idno>
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<term>Human</term>
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<term>Severe acute respiratory syndrome</term>
<term>Virology</term>
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<term>Homme</term>
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<front><div type="abstract" xml:lang="en">Studies of patients with severe acute respiratory syndrome (SARS) demonstrate that the respiratory tract is a major site of SARS-coronavirus (CoV) infection and disease morbidity. We studied host-pathogen interactions using native lung tissue and a model of well-differentiated cultures of primary human airway epithelia. Angiotensin converting enzyme 2 (ACE2), the receptor for both the SARS-CoV and the related human respiratory coronavirus NL63, was expressed in human airway epithelia as well as lung parenchyma. As assessed by immunofluorescence staining and membrane biotinylation, ACE2 protein was more abundantly expressed on the apical than the basolateral surface of polarized airway epithelia. Interestingly, ACE2 expression positively correlated with the differentiation state of epithelia. Undifferentiated cells expressing little ACE2 were poorly infected with SARS-CoV, while well-differentiated cells expressing more ACE2 were readily infected. Expression of ACE2 in poorly differentiated epithelia facilitated SARS spike (S) protein-pseudotyped virus entry. Consistent with the expression pattern of ACE2, the entry of SARS-CoV or a lentivirus pseudotyped with SARS-CoV S protein in differentiated epithelia was more efficient when applied to the apical surface. Furthermore, SARS-CoV replicated in polarized epithelia and preferentially exited via the apical surface. The results indicate that infection of human airway epithelia by SARS coronavirus correlates with the state of cell differentiation and ACE2 expression and localization. These findings have implications for understanding disease pathogenesis associated with SARS-CoV and NL63 infections.</div>
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<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
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<fA14 i1="03"><s1>Department of Microbiology and Molecular Genetics, Harvard University</s1>
<s2>Cambridge, Massachusetts 02138</s2>
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<sZ>7 aut.</sZ>
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<s1>© 2006 INIST-CNRS. All rights reserved.</s1>
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<server><NO>PASCAL 06-0013780 INIST</NO>
<ET>ACE2 receptor expression and severe acute respiratory syndrome coronavirus infection depend on differentiation of human airway epithelia</ET>
<AU>HONG PENG JIA; LOOK (Dwight C.); LEI SHI; HICKEY (Melissa); PEWE (Lecia); NETLAND (Jason); FARZAN (Michael); WOHLFORD-LENANE (Christine); PERLMAN (Stanley); MCCRAY (Paul B. JR)</AU>
<AF>Department of Pediatrics, Carver College of Medicine, University of Iowa/Iowa City, Iowa 52242/Etats-Unis (1 aut., 4 aut., 5 aut., 6 aut., 8 aut., 9 aut., 10 aut.); Department of Internal Medicine, Carver College of Medicine, University of Iowa/Iowa City, Iowa 52242/Etats-Unis (2 aut., 3 aut.); Department of Microbiology and Molecular Genetics, Harvard University/Cambridge, Massachusetts 02138/Etats-Unis (7 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2005; Vol. 79; No. 23; Pp. 14614-14621; Bibl. 49 ref.</SO>
<LA>Anglais</LA>
<EA>Studies of patients with severe acute respiratory syndrome (SARS) demonstrate that the respiratory tract is a major site of SARS-coronavirus (CoV) infection and disease morbidity. We studied host-pathogen interactions using native lung tissue and a model of well-differentiated cultures of primary human airway epithelia. Angiotensin converting enzyme 2 (ACE2), the receptor for both the SARS-CoV and the related human respiratory coronavirus NL63, was expressed in human airway epithelia as well as lung parenchyma. As assessed by immunofluorescence staining and membrane biotinylation, ACE2 protein was more abundantly expressed on the apical than the basolateral surface of polarized airway epithelia. Interestingly, ACE2 expression positively correlated with the differentiation state of epithelia. Undifferentiated cells expressing little ACE2 were poorly infected with SARS-CoV, while well-differentiated cells expressing more ACE2 were readily infected. Expression of ACE2 in poorly differentiated epithelia facilitated SARS spike (S) protein-pseudotyped virus entry. Consistent with the expression pattern of ACE2, the entry of SARS-CoV or a lentivirus pseudotyped with SARS-CoV S protein in differentiated epithelia was more efficient when applied to the apical surface. Furthermore, SARS-CoV replicated in polarized epithelia and preferentially exited via the apical surface. The results indicate that infection of human airway epithelia by SARS coronavirus correlates with the state of cell differentiation and ACE2 expression and localization. These findings have implications for understanding disease pathogenesis associated with SARS-CoV and NL63 infections.</EA>
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<FD>Coronavirus; Homme; Voie respiratoire; Microbiologie; Virologie; Syndrome respiratoire aigu sévère</FD>
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<ED>Coronavirus; Human; Respiratory tract; Microbiology; Virology; Severe acute respiratory syndrome</ED>
<EG>Coronaviridae; Nidovirales; Virus; Respiratory disease; Viral disease; Infection; Lung disease; Respiratory system</EG>
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ACE2 receptor expression and severe acute respiratory syndrome coronavirus infection depend on differentiation of human airway epithelia

ACE2 receptor expression and severe acute respiratory syndrome coronavirus infection depend on differentiation of human airway epithelia

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