Severe acute respiratory syndrome coronavirus infection of human ciliated airway epithelia : Role of ciliated cells in viral spread in the conducting airways of the lungs
Identifieur interne : 000561 ( PascalFrancis/Corpus ); précédent : 000560; suivant : 000562Severe acute respiratory syndrome coronavirus infection of human ciliated airway epithelia : Role of ciliated cells in viral spread in the conducting airways of the lungs
Auteurs : Amy C. Sims ; Ralph S. Baric ; Boyd Yount ; Susan E. Burkett ; Peter L. Collins ; Raymond J. PicklesSource :
- Journal of virology [ 0022-538X ] ; 2005.
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Abstract
Severe acute respiratory syndrome coronavirus (SARS-CoV) emerged in 2002 as an important cause of severe lower respiratory tract infection in humans, and in vitro models of the lung are needed to elucidate cellular targets and the consequences of viral infection. The SARS-CoV receptor, human angiotensin 1-converting enzyme 2 (hACE2), was detected in ciliated airway epithelial cells of human airway tissues derived from nasal or tracheobronchial regions, suggesting that SARS-CoV may infect the proximal airways. To assess infectivity in an in vitro model of human ciliated airway epithelia (HAE) derived from nasal and tracheobronchial airway regions, we generated recombinant SARS-CoV by deletion of open reading frame 7a/7b (ORF7a/ 7b) and insertion of the green fluorescent protein (GFP), resulting in SARS-CoV GFP. SARS-CoV GFP replicated to titers similar to those of wild-type viruses in cell lines. SARS-CoV specifically infected HAE via the apical surface and replicated to titers of 107 PFU/ml by 48 h postinfection. Polyclonal antisera directed against hACE2 blocked virus infection and replication, suggesting that hACE2 is the primary receptor for SARS-CoV infection of HAE. SARS-CoV structural proteins and virions localized to ciliated epithelial cells. Infection was highly cytolytic, as infected ciliated cells were necrotic and shed over time onto the luminal surface of the epithelium. SARS-CoV GFP also replicated to a lesser extent in ciliated cell cultures derived from hamster or rhesus monkey airways. Efficient SARS-CoV infection of ciliated cells in HAE provides a useful in vitro model of human lung origin to study characteristics of SARS-CoV replication and pathogenesis.
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Format Inist (serveur)
| NO : | PASCAL 06-0040428 INIST |
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| ET : | Severe acute respiratory syndrome coronavirus infection of human ciliated airway epithelia : Role of ciliated cells in viral spread in the conducting airways of the lungs |
| AU : | SIMS (Amy C.); BARIC (Ralph S.); YOUNT (Boyd); BURKETT (Susan E.); COLLINS (Peter L.); PICKLES (Raymond J.) |
| AF : | Department of Epidemiology, University of North Carolina at Chapel Hill/Chapel Hill, North Carolina/Etats-Unis (1 aut., 2 aut., 3 aut.); Department of Microbiology and Immunology, University of North Carolina at Chapel Hill/Chapel Hill, North Carolina/Etats-Unis (2 aut., 6 aut.); Cystic Fibrosis/Pulmonary Research and Treatment Center, University of North Carolina at Chapel Hill/Chapel Hill, North Carolina/Etats-Unis (4 aut., 6 aut.); Respiratory Viruses Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health/Bethesda, Maryland/Etats-Unis (5 aut.) |
| DT : | Publication en série; Niveau analytique |
| SO : | Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2005; Vol. 79; No. 24; Pp. 15511-15524; Bibl. 75 ref. |
| LA : | Anglais |
| EA : | Severe acute respiratory syndrome coronavirus (SARS-CoV) emerged in 2002 as an important cause of severe lower respiratory tract infection in humans, and in vitro models of the lung are needed to elucidate cellular targets and the consequences of viral infection. The SARS-CoV receptor, human angiotensin 1-converting enzyme 2 (hACE2), was detected in ciliated airway epithelial cells of human airway tissues derived from nasal or tracheobronchial regions, suggesting that SARS-CoV may infect the proximal airways. To assess infectivity in an in vitro model of human ciliated airway epithelia (HAE) derived from nasal and tracheobronchial airway regions, we generated recombinant SARS-CoV by deletion of open reading frame 7a/7b (ORF7a/ 7b) and insertion of the green fluorescent protein (GFP), resulting in SARS-CoV GFP. SARS-CoV GFP replicated to titers similar to those of wild-type viruses in cell lines. SARS-CoV specifically infected HAE via the apical surface and replicated to titers of 107 PFU/ml by 48 h postinfection. Polyclonal antisera directed against hACE2 blocked virus infection and replication, suggesting that hACE2 is the primary receptor for SARS-CoV infection of HAE. SARS-CoV structural proteins and virions localized to ciliated epithelial cells. Infection was highly cytolytic, as infected ciliated cells were necrotic and shed over time onto the luminal surface of the epithelium. SARS-CoV GFP also replicated to a lesser extent in ciliated cell cultures derived from hamster or rhesus monkey airways. Efficient SARS-CoV infection of ciliated cells in HAE provides a useful in vitro model of human lung origin to study characteristics of SARS-CoV replication and pathogenesis. |
| CC : | 002A05C10 |
| FD : | Coronavirus; Homme; Voie respiratoire; Microbiologie; Virologie; Syndrome respiratoire aigu sévère |
| FG : | Coronaviridae; Nidovirales; Virus; Poumon pathologie; Virose; Infection; Appareil respiratoire pathologie; Appareil respiratoire |
| ED : | Coronavirus; Human; Respiratory tract; Microbiology; Virology; Severe acute respiratory syndrome |
| EG : | Coronaviridae; Nidovirales; Virus; Lung disease; Viral disease; Infection; Respiratory disease; Respiratory system |
| SD : | Coronavirus; Hombre; Vía respiratoria; Microbiología; Virología; Síndrome respiratorio agudo severo |
| LO : | INIST-13592.354000134506980520 |
| ID : | 06-0040428 |
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Burkett</name><affiliation><inist:fA14 i1="03"><s1>Cystic Fibrosis/Pulmonary Research and Treatment Center, University of North Carolina at Chapel Hill</s1><s2>Chapel Hill, North Carolina</s2><s3>USA</s3><sZ>4 aut.</sZ><sZ>6 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Collins, Peter L" sort="Collins, Peter L" uniqKey="Collins P" first="Peter L." last="Collins">Peter L. Collins</name><affiliation><inist:fA14 i1="04"><s1>Respiratory Viruses Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health</s1><s2>Bethesda, Maryland</s2><s3>USA</s3><sZ>5 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Pickles, Raymond J" sort="Pickles, Raymond J" uniqKey="Pickles R" first="Raymond J." last="Pickles">Raymond J. Pickles</name><affiliation><inist:fA14 i1="02"><s1>Department of Microbiology and Immunology, University of North Carolina at Chapel Hill</s1><s2>Chapel Hill, North Carolina</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>6 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="03"><s1>Cystic Fibrosis/Pulmonary Research and Treatment Center, University of North Carolina at Chapel Hill</s1><s2>Chapel Hill, North Carolina</s2><s3>USA</s3><sZ>4 aut.</sZ><sZ>6 aut.</sZ></inist:fA14></affiliation></author></analytic><series><title level="j" type="main">Journal of virology</title><title level="j" type="abbreviated">J. virol.</title><idno type="ISSN">0022-538X</idno><imprint><date when="2005">2005</date></imprint></series></biblStruct></sourceDesc><seriesStmt><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>Coronavirus</term><term>Human</term><term>Microbiology</term><term>Respiratory tract</term><term>Severe acute respiratory syndrome</term><term>Virology</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Coronavirus</term><term>Homme</term><term>Voie respiratoire</term><term>Microbiologie</term><term>Virologie</term><term>Syndrome respiratoire aigu sévère</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome coronavirus (SARS-CoV) emerged in 2002 as an important cause of severe lower respiratory tract infection in humans, and in vitro models of the lung are needed to elucidate cellular targets and the consequences of viral infection. The SARS-CoV receptor, human angiotensin 1-converting enzyme 2 (hACE2), was detected in ciliated airway epithelial cells of human airway tissues derived from nasal or tracheobronchial regions, suggesting that SARS-CoV may infect the proximal airways. To assess infectivity in an in vitro model of human ciliated airway epithelia (HAE) derived from nasal and tracheobronchial airway regions, we generated recombinant SARS-CoV by deletion of open reading frame 7a/7b (ORF7a/ 7b) and insertion of the green fluorescent protein (GFP), resulting in SARS-CoV GFP. SARS-CoV GFP replicated to titers similar to those of wild-type viruses in cell lines. SARS-CoV specifically infected HAE via the apical surface and replicated to titers of 10<sup>7</sup> PFU/ml by 48 h postinfection. Polyclonal antisera directed against hACE2 blocked virus infection and replication, suggesting that hACE2 is the primary receptor for SARS-CoV infection of HAE. SARS-CoV structural proteins and virions localized to ciliated epithelial cells. Infection was highly cytolytic, as infected ciliated cells were necrotic and shed over time onto the luminal surface of the epithelium. SARS-CoV GFP also replicated to a lesser extent in ciliated cell cultures derived from hamster or rhesus monkey airways. Efficient SARS-CoV infection of ciliated cells in HAE provides a useful in vitro model of human lung origin to study characteristics of SARS-CoV replication and pathogenesis.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0022-538X</s0></fA01><fA03 i2="1"><s0>J. virol.</s0></fA03><fA05><s2>79</s2></fA05><fA06><s2>24</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Severe acute respiratory syndrome coronavirus infection of human ciliated airway epithelia : Role of ciliated cells in viral spread in the conducting airways of the lungs</s1></fA08><fA11 i1="01" i2="1"><s1>SIMS (Amy C.)</s1></fA11><fA11 i1="02" i2="1"><s1>BARIC (Ralph S.)</s1></fA11><fA11 i1="03" i2="1"><s1>YOUNT (Boyd)</s1></fA11><fA11 i1="04" i2="1"><s1>BURKETT (Susan E.)</s1></fA11><fA11 i1="05" i2="1"><s1>COLLINS (Peter L.)</s1></fA11><fA11 i1="06" i2="1"><s1>PICKLES (Raymond J.)</s1></fA11><fA14 i1="01"><s1>Department of Epidemiology, University of North Carolina at Chapel Hill</s1><s2>Chapel Hill, North Carolina</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ></fA14><fA14 i1="02"><s1>Department of Microbiology and Immunology, University of North Carolina at Chapel Hill</s1><s2>Chapel Hill, North Carolina</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>6 aut.</sZ></fA14><fA14 i1="03"><s1>Cystic Fibrosis/Pulmonary Research and Treatment Center, University of North Carolina at Chapel Hill</s1><s2>Chapel Hill, North Carolina</s2><s3>USA</s3><sZ>4 aut.</sZ><sZ>6 aut.</sZ></fA14><fA14 i1="04"><s1>Respiratory Viruses Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health</s1><s2>Bethesda, Maryland</s2><s3>USA</s3><sZ>5 aut.</sZ></fA14><fA20><s1>15511-15524</s1></fA20><fA21><s1>2005</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>13592</s2><s5>354000134506980520</s5></fA43><fA44><s0>0000</s0><s1>© 2006 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>75 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>06-0040428</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Journal of virology</s0></fA64><fA66 i1="01"><s0>USA</s0></fA66><fC01 i1="01" l="ENG"><s0>Severe acute respiratory syndrome coronavirus (SARS-CoV) emerged in 2002 as an important cause of severe lower respiratory tract infection in humans, and in vitro models of the lung are needed to elucidate cellular targets and the consequences of viral infection. The SARS-CoV receptor, human angiotensin 1-converting enzyme 2 (hACE2), was detected in ciliated airway epithelial cells of human airway tissues derived from nasal or tracheobronchial regions, suggesting that SARS-CoV may infect the proximal airways. To assess infectivity in an in vitro model of human ciliated airway epithelia (HAE) derived from nasal and tracheobronchial airway regions, we generated recombinant SARS-CoV by deletion of open reading frame 7a/7b (ORF7a/ 7b) and insertion of the green fluorescent protein (GFP), resulting in SARS-CoV GFP. SARS-CoV GFP replicated to titers similar to those of wild-type viruses in cell lines. SARS-CoV specifically infected HAE via the apical surface and replicated to titers of 10<sup>7</sup> PFU/ml by 48 h postinfection. Polyclonal antisera directed against hACE2 blocked virus infection and replication, suggesting that hACE2 is the primary receptor for SARS-CoV infection of HAE. SARS-CoV structural proteins and virions localized to ciliated epithelial cells. Infection was highly cytolytic, as infected ciliated cells were necrotic and shed over time onto the luminal surface of the epithelium. SARS-CoV GFP also replicated to a lesser extent in ciliated cell cultures derived from hamster or rhesus monkey airways. 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The SARS-CoV receptor, human angiotensin 1-converting enzyme 2 (hACE2), was detected in ciliated airway epithelial cells of human airway tissues derived from nasal or tracheobronchial regions, suggesting that SARS-CoV may infect the proximal airways. To assess infectivity in an in vitro model of human ciliated airway epithelia (HAE) derived from nasal and tracheobronchial airway regions, we generated recombinant SARS-CoV by deletion of open reading frame 7a/7b (ORF7a/ 7b) and insertion of the green fluorescent protein (GFP), resulting in SARS-CoV GFP. SARS-CoV GFP replicated to titers similar to those of wild-type viruses in cell lines. SARS-CoV specifically infected HAE via the apical surface and replicated to titers of 10<sup>7</sup> PFU/ml by 48 h postinfection. Polyclonal antisera directed against hACE2 blocked virus infection and replication, suggesting that hACE2 is the primary receptor for SARS-CoV infection of HAE. SARS-CoV structural proteins and virions localized to ciliated epithelial cells. Infection was highly cytolytic, as infected ciliated cells were necrotic and shed over time onto the luminal surface of the epithelium. SARS-CoV GFP also replicated to a lesser extent in ciliated cell cultures derived from hamster or rhesus monkey airways. Efficient SARS-CoV infection of ciliated cells in HAE provides a useful in vitro model of human lung origin to study characteristics of SARS-CoV replication and pathogenesis.</EA><CC>002A05C10</CC><FD>Coronavirus; Homme; Voie respiratoire; Microbiologie; Virologie; Syndrome respiratoire aigu sévère</FD><FG>Coronaviridae; Nidovirales; Virus; Poumon pathologie; Virose; Infection; Appareil respiratoire pathologie; Appareil respiratoire</FG><ED>Coronavirus; Human; Respiratory tract; Microbiology; Virology; Severe acute respiratory syndrome</ED><EG>Coronaviridae; Nidovirales; Virus; Lung disease; Viral disease; Infection; Respiratory disease; Respiratory system</EG><SD>Coronavirus; Hombre; Vía respiratoria; Microbiología; Virología; Síndrome respiratorio agudo severo</SD><LO>INIST-13592.354000134506980520</LO><ID>06-0040428</ID></server></inist></record>Pour manipuler ce document sous Unix (Dilib)
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