siRNA silencing of angiotensin-converting enzyme 2 reduced severe acute respiratory syndrome-associated coronavirus replications in Vero E6 cells.
Identifieur interne : 001958 ( PubMed/Checkpoint ); précédent : 001957; suivant : 001959siRNA silencing of angiotensin-converting enzyme 2 reduced severe acute respiratory syndrome-associated coronavirus replications in Vero E6 cells.
Auteurs : C-Y Lu [Taïwan] ; H-Y Huang ; T-H Yang ; L-Y Chang ; C-Y Lee ; L-M HuangSource :
- European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology [ 0934-9723 ] ; 2008.
Descripteurs français
- KwdFr :
- MESH :
- génétique : Peptidyl-Dipeptidase A.
- métabolisme : Peptidyl-Dipeptidase A.
- pharmacologie : Petit ARN interférent.
- physiologie : Virus du SRAS.
- Animaux, Cellules Vero, Chats, Extinction de l'expression des gènes, Lignée cellulaire, Réplication virale, Virus du SRAS.
English descriptors
- KwdEn :
- MESH :
- chemical , genetics : Peptidyl-Dipeptidase A.
- drug effects : Gene Silencing, SARS Virus, Virus Replication.
- chemical , metabolism : Peptidyl-Dipeptidase A.
- chemical , pharmacology : RNA, Small Interfering.
- physiology : SARS Virus.
- Animals, Cats, Cell Line, Chlorocebus aethiops, Vero Cells.
Abstract
The outbreak of severe acute respiratory syndrome (SARS) in 2002-2003 has had a significant impact worldwide. No effective prophylaxis or treatment for SARS is available up to now. Angiotensin-converting enzyme 2 (ACE2) is the cellular receptor for SARS-associated coronavirus (SARS-CoV). By expressing a U6 promoter-driven small interfering RNA containing sequences homologous to part of ACE2 mRNA, we successfully silenced ACE2 expression in Vero E6 cells. By detecting negative strand SARS-CoV RNA and measuring RNA copy numbers of SARS-CoV by real-time reverse transcription polymerase chain reaction (RT-PCR), we demonstrated that SARS-CoV infection was reduced in the ACE2-silenced cell lines. These findings support the involvement of ACE2 in SARS-CoV infections and provide a basis for further studies on potential use of siRNA targeting ACE2 as a preventive or therapeutic strategy for SARS.
DOI: 10.1007/s10096-008-0495-5
PubMed: 18449585
Affiliations:
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sortKey="Chang, L Y" sort="Chang, L Y" uniqKey="Chang L" first="L-Y" last="Chang">L-Y Chang</name></author><author><name sortKey="Lee, C Y" sort="Lee, C Y" uniqKey="Lee C" first="C-Y" last="Lee">C-Y Lee</name></author><author><name sortKey="Huang, L M" sort="Huang, L M" uniqKey="Huang L" first="L-M" last="Huang">L-M Huang</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2008">2008</date><idno type="RBID">pubmed:18449585</idno><idno type="pmid">18449585</idno><idno type="doi">10.1007/s10096-008-0495-5</idno><idno type="wicri:Area/PubMed/Corpus">001B53</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001B53</idno><idno type="wicri:Area/PubMed/Curation">001B53</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">001B53</idno><idno type="wicri:Area/PubMed/Checkpoint">001958</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">001958</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">siRNA silencing of angiotensin-converting enzyme 2 reduced severe acute respiratory syndrome-associated coronavirus replications in Vero E6 cells.</title><author><name sortKey="Lu, C Y" sort="Lu, C Y" uniqKey="Lu C" first="C-Y" last="Lu">C-Y Lu</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pediatrics, National Taiwan University Hospital, No. 7, Chung-Shan South Road, Taipei, Taiwan. cylu@ntuh.gov.tw</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Pediatrics, National Taiwan University Hospital, No. 7, Chung-Shan South Road, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation></author><author><name sortKey="Huang, H Y" sort="Huang, H Y" uniqKey="Huang H" first="H-Y" last="Huang">H-Y Huang</name></author><author><name sortKey="Yang, T H" sort="Yang, T H" uniqKey="Yang T" first="T-H" last="Yang">T-H Yang</name></author><author><name sortKey="Chang, L Y" sort="Chang, L Y" uniqKey="Chang L" first="L-Y" last="Chang">L-Y Chang</name></author><author><name sortKey="Lee, C Y" sort="Lee, C Y" uniqKey="Lee C" first="C-Y" last="Lee">C-Y Lee</name></author><author><name sortKey="Huang, L M" sort="Huang, L M" uniqKey="Huang L" first="L-M" last="Huang">L-M Huang</name></author></analytic><series><title level="j">European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology</title><idno type="ISSN">0934-9723</idno><imprint><date when="2008" type="published">2008</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Cats</term><term>Cell Line</term><term>Chlorocebus aethiops</term><term>Gene Silencing (drug effects)</term><term>Peptidyl-Dipeptidase A (genetics)</term><term>Peptidyl-Dipeptidase A (metabolism)</term><term>RNA, Small Interfering (pharmacology)</term><term>SARS Virus (drug effects)</term><term>SARS Virus (physiology)</term><term>Vero Cells</term><term>Virus Replication (drug effects)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Cellules Vero</term><term>Chats</term><term>Extinction de l'expression des gènes ()</term><term>Lignée cellulaire</term><term>Peptidyl-Dipeptidase A (génétique)</term><term>Peptidyl-Dipeptidase A (métabolisme)</term><term>Petit ARN interférent (pharmacologie)</term><term>Réplication virale ()</term><term>Virus du SRAS ()</term><term>Virus du SRAS (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Peptidyl-Dipeptidase A</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Gene Silencing</term><term>SARS Virus</term><term>Virus Replication</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Peptidyl-Dipeptidase A</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Peptidyl-Dipeptidase A</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Peptidyl-Dipeptidase A</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Petit ARN interférent</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>RNA, Small Interfering</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cats</term><term>Cell Line</term><term>Chlorocebus aethiops</term><term>Vero Cells</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules Vero</term><term>Chats</term><term>Extinction de l'expression des gènes</term><term>Lignée cellulaire</term><term>Réplication virale</term><term>Virus du SRAS</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The outbreak of severe acute respiratory syndrome (SARS) in 2002-2003 has had a significant impact worldwide. No effective prophylaxis or treatment for SARS is available up to now. Angiotensin-converting enzyme 2 (ACE2) is the cellular receptor for SARS-associated coronavirus (SARS-CoV). By expressing a U6 promoter-driven small interfering RNA containing sequences homologous to part of ACE2 mRNA, we successfully silenced ACE2 expression in Vero E6 cells. By detecting negative strand SARS-CoV RNA and measuring RNA copy numbers of SARS-CoV by real-time reverse transcription polymerase chain reaction (RT-PCR), we demonstrated that SARS-CoV infection was reduced in the ACE2-silenced cell lines. These findings support the involvement of ACE2 in SARS-CoV infections and provide a basis for further studies on potential use of siRNA targeting ACE2 as a preventive or therapeutic strategy for SARS.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">18449585</PMID><DateCompleted><Year>2008</Year><Month>12</Month><Day>12</Day></DateCompleted><DateRevised><Year>2020</Year><Month>03</Month><Day>24</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0934-9723</ISSN><JournalIssue CitedMedium="Print"><Volume>27</Volume><Issue>8</Issue><PubDate><Year>2008</Year><Month>Aug</Month></PubDate></JournalIssue><Title>European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology</Title><ISOAbbreviation>Eur. J. Clin. Microbiol. Infect. 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By detecting negative strand SARS-CoV RNA and measuring RNA copy numbers of SARS-CoV by real-time reverse transcription polymerase chain reaction (RT-PCR), we demonstrated that SARS-CoV infection was reduced in the ACE2-silenced cell lines. These findings support the involvement of ACE2 in SARS-CoV infections and provide a basis for further studies on potential use of siRNA targeting ACE2 as a preventive or therapeutic strategy for SARS.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lu</LastName><ForeName>C-Y</ForeName><Initials>CY</Initials><AffiliationInfo><Affiliation>Department of Pediatrics, National Taiwan University Hospital, No. 7, Chung-Shan South Road, Taipei, Taiwan. cylu@ntuh.gov.tw</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Huang</LastName><ForeName>H-Y</ForeName><Initials>HY</Initials></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>T-H</ForeName><Initials>TH</Initials></Author><Author ValidYN="Y"><LastName>Chang</LastName><ForeName>L-Y</ForeName><Initials>LY</Initials></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>C-Y</ForeName><Initials>CY</Initials></Author><Author 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