The 3a protein of severe acute respiratory syndrome-associated coronavirus induces apoptosis in Vero E6 cells.
Identifieur interne : 002685 ( PubMed/Curation ); précédent : 002684; suivant : 002686The 3a protein of severe acute respiratory syndrome-associated coronavirus induces apoptosis in Vero E6 cells.
Auteurs : Patrick T W. Law [République populaire de Chine] ; Chi-Hang Wong [République populaire de Chine] ; Thomas C C. Au [République populaire de Chine] ; Chi-Pang Chuck [République populaire de Chine] ; Siu-Kai Kong [République populaire de Chine] ; Paul K S. Chan [République populaire de Chine] ; Ka-Fai To [République populaire de Chine] ; Anthony W I. Lo [République populaire de Chine] ; Judy Y W. Chan [République populaire de Chine] ; Yick-Keung Suen [République populaire de Chine] ; H Y Edwin Chan [République populaire de Chine] ; Kwok-Pui Fung [République populaire de Chine] ; Mary M Y. Waye [République populaire de Chine] ; Joseph J Y. Sung [République populaire de Chine] ; Y M Dennis Lo [République populaire de Chine] ; Stephen K W. Tsui [République populaire de Chine]Source :
- The Journal of general virology [ 0022-1317 ] ; 2005.
Descripteurs français
- KwdFr :
- Animaux, Apoptose, Cellules Vero, Humains, Intestins (virologie), Muqueuse intestinale (métabolisme), Poumon (métabolisme), Poumon (virologie), Protéines virales (métabolisme), Réticulum endoplasmique (métabolisme), Réticulum endoplasmique (virologie), Syndrome respiratoire aigu sévère (virologie), Virus du SRAS (métabolisme), Virus du SRAS (pathogénicité).
- MESH :
- métabolisme : Muqueuse intestinale, Poumon, Protéines virales, Réticulum endoplasmique, Virus du SRAS.
- pathogénicité : Virus du SRAS.
- virologie : Intestins, Poumon, Réticulum endoplasmique, Syndrome respiratoire aigu sévère.
- Animaux, Apoptose, Cellules Vero, Humains.
English descriptors
- KwdEn :
- Animals, Apoptosis, Chlorocebus aethiops, Endoplasmic Reticulum (metabolism), Endoplasmic Reticulum (virology), Humans, Intestinal Mucosa (metabolism), Intestines (virology), Lung (metabolism), Lung (virology), SARS Virus (metabolism), SARS Virus (pathogenicity), Severe Acute Respiratory Syndrome (virology), Vero Cells, Viral Proteins (metabolism).
- MESH :
- chemical , metabolism : Viral Proteins.
- metabolism : Endoplasmic Reticulum, Intestinal Mucosa, Lung, SARS Virus.
- pathogenicity : SARS Virus.
- virology : Endoplasmic Reticulum, Intestines, Lung, Severe Acute Respiratory Syndrome.
- Animals, Apoptosis, Chlorocebus aethiops, Humans, Vero Cells.
Abstract
An outbreak of severe acute respiratory syndrome (SARS) occurred in China and the first case emerged in mid-November 2002. The aetiological agent of this disease was found to be a previously unknown coronavirus, SARS-associated coronavirus (SARS-CoV). The detailed pathology of SARS-CoV infection and the host response to the viral infection are still not known. The 3a gene encodes a non-structural viral protein, which is predicted to be a transmembrane protein. In this study, it was shown that the 3a protein was expressed in the lungs and intestinal tissues of SARS patients and that the protein localized to the endoplasmic reticulum in 3a-transfected monkey kidney Vero E6 cells. In vitro experiments of chromatin condensation and DNA fragmentation suggested that the 3a protein may trigger apoptosis. These data showed that overexpression of a single SARS-CoV protein can induce apoptosis in vitro.
DOI: 10.1099/vir.0.80813-0
PubMed: 15958670
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<author><name sortKey="Chan, H Y Edwin" sort="Chan, H Y Edwin" uniqKey="Chan H" first="H Y Edwin" last="Chan">H Y Edwin Chan</name>
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<front><div type="abstract" xml:lang="en">An outbreak of severe acute respiratory syndrome (SARS) occurred in China and the first case emerged in mid-November 2002. The aetiological agent of this disease was found to be a previously unknown coronavirus, SARS-associated coronavirus (SARS-CoV). The detailed pathology of SARS-CoV infection and the host response to the viral infection are still not known. The 3a gene encodes a non-structural viral protein, which is predicted to be a transmembrane protein. In this study, it was shown that the 3a protein was expressed in the lungs and intestinal tissues of SARS patients and that the protein localized to the endoplasmic reticulum in 3a-transfected monkey kidney Vero E6 cells. In vitro experiments of chromatin condensation and DNA fragmentation suggested that the 3a protein may trigger apoptosis. These data showed that overexpression of a single SARS-CoV protein can induce apoptosis in vitro.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">15958670</PMID>
<DateCompleted><Year>2005</Year>
<Month>07</Month>
<Day>28</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>03</Month>
<Day>06</Day>
</DateRevised>
<Article PubModel="Print"><Journal><ISSN IssnType="Print">0022-1317</ISSN>
<JournalIssue CitedMedium="Print"><Volume>86</Volume>
<Issue>Pt 7</Issue>
<PubDate><Year>2005</Year>
<Month>Jul</Month>
</PubDate>
</JournalIssue>
<Title>The Journal of general virology</Title>
<ISOAbbreviation>J. Gen. Virol.</ISOAbbreviation>
</Journal>
<ArticleTitle>The 3a protein of severe acute respiratory syndrome-associated coronavirus induces apoptosis in Vero E6 cells.</ArticleTitle>
<Pagination><MedlinePgn>1921-1930</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1099/vir.0.80813-0</ELocationID>
<Abstract><AbstractText>An outbreak of severe acute respiratory syndrome (SARS) occurred in China and the first case emerged in mid-November 2002. The aetiological agent of this disease was found to be a previously unknown coronavirus, SARS-associated coronavirus (SARS-CoV). The detailed pathology of SARS-CoV infection and the host response to the viral infection are still not known. The 3a gene encodes a non-structural viral protein, which is predicted to be a transmembrane protein. In this study, it was shown that the 3a protein was expressed in the lungs and intestinal tissues of SARS patients and that the protein localized to the endoplasmic reticulum in 3a-transfected monkey kidney Vero E6 cells. In vitro experiments of chromatin condensation and DNA fragmentation suggested that the 3a protein may trigger apoptosis. These data showed that overexpression of a single SARS-CoV protein can induce apoptosis in vitro.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Law</LastName>
<ForeName>Patrick T W</ForeName>
<Initials>PTW</Initials>
<AffiliationInfo><Affiliation>Department of Biochemistry, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Centre for Emerging Infectious Diseases, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wong</LastName>
<ForeName>Chi-Hang</ForeName>
<Initials>CH</Initials>
<AffiliationInfo><Affiliation>Centre for Emerging Infectious Diseases, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Au</LastName>
<ForeName>Thomas C C</ForeName>
<Initials>TCC</Initials>
<AffiliationInfo><Affiliation>Centre for Emerging Infectious Diseases, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chuck</LastName>
<ForeName>Chi-Pang</ForeName>
<Initials>CP</Initials>
<AffiliationInfo><Affiliation>Department of Biochemistry, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kong</LastName>
<ForeName>Siu-Kai</ForeName>
<Initials>SK</Initials>
<AffiliationInfo><Affiliation>Department of Biochemistry, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chan</LastName>
<ForeName>Paul K S</ForeName>
<Initials>PKS</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>To</LastName>
<ForeName>Ka-Fai</ForeName>
<Initials>KF</Initials>
<AffiliationInfo><Affiliation>Department of Anatomical and Cellular Pathology, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lo</LastName>
<ForeName>Anthony W I</ForeName>
<Initials>AWI</Initials>
<AffiliationInfo><Affiliation>Department of Anatomical and Cellular Pathology, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chan</LastName>
<ForeName>Judy Y W</ForeName>
<Initials>JYW</Initials>
<AffiliationInfo><Affiliation>Department of Biochemistry, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Suen</LastName>
<ForeName>Yick-Keung</ForeName>
<Initials>YK</Initials>
<AffiliationInfo><Affiliation>Department of Biochemistry, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chan</LastName>
<ForeName>H Y Edwin</ForeName>
<Initials>HYE</Initials>
<AffiliationInfo><Affiliation>Department of Biochemistry, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Fung</LastName>
<ForeName>Kwok-Pui</ForeName>
<Initials>KP</Initials>
<AffiliationInfo><Affiliation>The Croucher Laboratory for Human Genomics, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Biochemistry, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Waye</LastName>
<ForeName>Mary M Y</ForeName>
<Initials>MMY</Initials>
<AffiliationInfo><Affiliation>The Croucher Laboratory for Human Genomics, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Biochemistry, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sung</LastName>
<ForeName>Joseph J Y</ForeName>
<Initials>JJY</Initials>
<AffiliationInfo><Affiliation>Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Centre for Emerging Infectious Diseases, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lo</LastName>
<ForeName>Y M Dennis</ForeName>
<Initials>YMD</Initials>
<AffiliationInfo><Affiliation>Department of Chemical Pathology, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Centre for Emerging Infectious Diseases, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Tsui</LastName>
<ForeName>Stephen K W</ForeName>
<Initials>SKW</Initials>
<AffiliationInfo><Affiliation>The Croucher Laboratory for Human Genomics, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Biochemistry, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Centre for Emerging Infectious Diseases, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
</Article>
<MedlineJournalInfo><Country>England</Country>
<MedlineTA>J Gen Virol</MedlineTA>
<NlmUniqueID>0077340</NlmUniqueID>
<ISSNLinking>0022-1317</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C487105">3a protein, severe acute respiratory syndrome coronavirus</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D014764">Viral Proteins</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017209" MajorTopicYN="Y">Apoptosis</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002522" MajorTopicYN="N">Chlorocebus aethiops</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004721" MajorTopicYN="N">Endoplasmic Reticulum</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007413" MajorTopicYN="N">Intestinal Mucosa</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007422" MajorTopicYN="N">Intestines</DescriptorName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008168" MajorTopicYN="N">Lung</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D045473" MajorTopicYN="N">SARS Virus</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000472" MajorTopicYN="Y">pathogenicity</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D045169" MajorTopicYN="N">Severe Acute Respiratory Syndrome</DescriptorName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014709" MajorTopicYN="N">Vero Cells</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014764" MajorTopicYN="N">Viral Proteins</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
</MeshHeadingList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2005</Year>
<Month>6</Month>
<Day>17</Day>
<Hour>9</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2005</Year>
<Month>7</Month>
<Day>29</Day>
<Hour>9</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2005</Year>
<Month>6</Month>
<Day>17</Day>
<Hour>9</Hour>
<Minute>0</Minute>
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</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">15958670</ArticleId>
<ArticleId IdType="doi">10.1099/vir.0.80813-0</ArticleId>
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