Apical entry and release of severe acute respiratory syndrome-associated coronavirus in polarized Calu-3 lung epithelial cells.
Identifieur interne : 002645 ( PubMed/Corpus ); précédent : 002644; suivant : 002646Apical 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. PetersSource :
- Journal of virology [ 0022-538X ] ; 2005.
English descriptors
- KwdEn :
- Antigens, Viral (metabolism), Cell Line, Tumor, Cell Polarity (physiology), Cytopathogenic Effect, Viral, Epithelial Cells (physiology), Epithelial Cells (virology), Fluorescent Antibody Technique, Humans, Lung, Receptors, Virus (metabolism), SARS Virus (growth & development), SARS Virus (metabolism), Severe Acute Respiratory Syndrome (virology).
- MESH :
- chemical , metabolism : Antigens, Viral, Receptors, Virus.
- growth & development : SARS Virus.
- metabolism : SARS Virus.
- physiology : Cell Polarity, Epithelial Cells.
- virology : Epithelial Cells, Severe Acute Respiratory Syndrome.
- Cell Line, Tumor, Cytopathogenic Effect, Viral, Fluorescent Antibody Technique, Humans, Lung.
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.
DOI: 10.1128/JVI.79.15.9470-9479.2005
PubMed: 16014910
Links to Exploration step
pubmed:16014910Le document en format XML
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Tseng</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, 77555-0609, USA. sktseng@utmb.edu</nlm:affiliation></affiliation></author><author><name sortKey="Tseng, Jennifer" sort="Tseng, Jennifer" uniqKey="Tseng J" first="Jennifer" last="Tseng">Jennifer Tseng</name></author><author><name sortKey="Perrone, Lucy" sort="Perrone, Lucy" uniqKey="Perrone L" first="Lucy" last="Perrone">Lucy Perrone</name></author><author><name sortKey="Worthy, Melissa" sort="Worthy, Melissa" uniqKey="Worthy M" first="Melissa" last="Worthy">Melissa Worthy</name></author><author><name sortKey="Popov, Vsevolod" sort="Popov, Vsevolod" uniqKey="Popov V" first="Vsevolod" last="Popov">Vsevolod Popov</name></author><author><name sortKey="Peters, Clarence J" sort="Peters, Clarence J" uniqKey="Peters C" first="Clarence J" last="Peters">Clarence J. 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Tseng</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, 77555-0609, USA. sktseng@utmb.edu</nlm:affiliation></affiliation></author><author><name sortKey="Tseng, Jennifer" sort="Tseng, Jennifer" uniqKey="Tseng J" first="Jennifer" last="Tseng">Jennifer Tseng</name></author><author><name sortKey="Perrone, Lucy" sort="Perrone, Lucy" uniqKey="Perrone L" first="Lucy" last="Perrone">Lucy Perrone</name></author><author><name sortKey="Worthy, Melissa" sort="Worthy, Melissa" uniqKey="Worthy M" first="Melissa" last="Worthy">Melissa Worthy</name></author><author><name sortKey="Popov, Vsevolod" sort="Popov, Vsevolod" uniqKey="Popov V" first="Vsevolod" last="Popov">Vsevolod Popov</name></author><author><name sortKey="Peters, Clarence J" sort="Peters, Clarence J" uniqKey="Peters C" first="Clarence J" last="Peters">Clarence J. Peters</name></author></analytic><series><title level="j">Journal of virology</title><idno type="ISSN">0022-538X</idno><imprint><date when="2005" type="published">2005</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antigens, Viral (metabolism)</term><term>Cell Line, Tumor</term><term>Cell Polarity (physiology)</term><term>Cytopathogenic Effect, Viral</term><term>Epithelial Cells (physiology)</term><term>Epithelial Cells (virology)</term><term>Fluorescent Antibody Technique</term><term>Humans</term><term>Lung</term><term>Receptors, Virus (metabolism)</term><term>SARS Virus (growth & development)</term><term>SARS Virus (metabolism)</term><term>Severe Acute Respiratory Syndrome (virology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Antigens, Viral</term><term>Receptors, Virus</term></keywords><keywords scheme="MESH" qualifier="growth & development" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Cell Polarity</term><term>Epithelial Cells</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Epithelial Cells</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line, Tumor</term><term>Cytopathogenic Effect, Viral</term><term>Fluorescent Antibody Technique</term><term>Humans</term><term>Lung</term></keywords></textClass></profileDesc></teiHeader><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></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16014910</PMID><DateCompleted><Year>2005</Year><Month>08</Month><Day>18</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0022-538X</ISSN><JournalIssue CitedMedium="Print"><Volume>79</Volume><Issue>15</Issue><PubDate><Year>2005</Year><Month>Aug</Month></PubDate></JournalIssue><Title>Journal of virology</Title><ISOAbbreviation>J. Virol.</ISOAbbreviation></Journal><ArticleTitle>Apical entry and release of severe acute respiratory syndrome-associated coronavirus in polarized Calu-3 lung epithelial cells.</ArticleTitle><Pagination><MedlinePgn>9470-9</MedlinePgn></Pagination><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tseng</LastName><ForeName>Chien-Te K</ForeName><Initials>CT</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, 77555-0609, USA. sktseng@utmb.edu</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tseng</LastName><ForeName>Jennifer</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Perrone</LastName><ForeName>Lucy</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Worthy</LastName><ForeName>Melissa</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Popov</LastName><ForeName>Vsevolod</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>Peters</LastName><ForeName>Clarence J</ForeName><Initials>CJ</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>N01AI25489</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>N01 AI 25489</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J 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