Replication-dependent downregulation of cellular angiotensin-converting enzyme 2 protein expression by human coronavirus NL63.
Identifieur interne : 001304 ( PubMed/Checkpoint ); précédent : 001303; suivant : 001305Replication-dependent downregulation of cellular angiotensin-converting enzyme 2 protein expression by human coronavirus NL63.
Auteurs : Ronald Dijkman [Pays-Bas] ; Maarten F. Jebbink [Pays-Bas] ; Martin Deijs [Pays-Bas] ; Aleksandra Milewska [Pays-Bas] ; Krzysztof Pyrc [Pologne] ; Elena Buelow [Pays-Bas] ; Anna Van Der Bijl [Pays-Bas] ; Lia Van Der Hoek [Pays-Bas]Source :
- The Journal of general virology [ 1465-2099 ] ; 2012.
Descripteurs français
- KwdFr :
- MESH :
- enzymologie : Infections à coronavirus.
- génétique : Coronavirus humain NL63, Peptidyl-Dipeptidase A.
- métabolisme : Peptidyl-Dipeptidase A.
- physiologie : Coronavirus humain NL63.
- virologie : Infections à coronavirus.
- Humains, Lignée cellulaire, Régulation négative, Réplication virale.
English descriptors
- KwdEn :
- MESH :
- chemical , genetics : Peptidyl-Dipeptidase A.
- enzymology : Coronavirus Infections.
- genetics : Coronavirus NL63, Human.
- chemical , metabolism : Peptidyl-Dipeptidase A.
- physiology : Coronavirus NL63, Human.
- virology : Coronavirus Infections.
- Cell Line, Down-Regulation, Humans, Virus Replication.
Abstract
Like severe acute respiratory syndrome coronavirus (SARS-CoV), human coronavirus (HCoV)-NL63 employs angiotensin-converting enzyme 2 (ACE2) as a receptor for cellular entry. SARS-CoV infection causes robust downregulation of cellular ACE2 expression levels and it has been suggested that the SARS-CoV effect on ACE2 is involved in the severity of disease. We investigated whether cellular ACE2 downregulation occurs at optimal replication conditions of HCoV-NL63 infection. The expression of the homologue of ACE2, the ACE protein not used as a receptor by HCoV-NL63, was measured as a control. A specific decrease for ACE2 protein level was observed when HCoV-NL63 was cultured at 34 °C. Culturing the virus at the suboptimal temperature of 37 °C resulted in low replication of the virus and the effect on ACE2 expression was lost. We conclude that the decline of ACE2 expression is dependent on the efficiency of HCoV-NL63 replication, and that HCoV-NL63 and SARS-CoV both affect cellular ACE2 expression during infection.
DOI: 10.1099/vir.0.043919-0
PubMed: 22718567
Affiliations:
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pubmed:22718567Le document en format XML
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<front><div type="abstract" xml:lang="en">Like severe acute respiratory syndrome coronavirus (SARS-CoV), human coronavirus (HCoV)-NL63 employs angiotensin-converting enzyme 2 (ACE2) as a receptor for cellular entry. SARS-CoV infection causes robust downregulation of cellular ACE2 expression levels and it has been suggested that the SARS-CoV effect on ACE2 is involved in the severity of disease. We investigated whether cellular ACE2 downregulation occurs at optimal replication conditions of HCoV-NL63 infection. The expression of the homologue of ACE2, the ACE protein not used as a receptor by HCoV-NL63, was measured as a control. A specific decrease for ACE2 protein level was observed when HCoV-NL63 was cultured at 34 °C. Culturing the virus at the suboptimal temperature of 37 °C resulted in low replication of the virus and the effect on ACE2 expression was lost. We conclude that the decline of ACE2 expression is dependent on the efficiency of HCoV-NL63 replication, and that HCoV-NL63 and SARS-CoV both affect cellular ACE2 expression during infection.</div>
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<Abstract><AbstractText>Like severe acute respiratory syndrome coronavirus (SARS-CoV), human coronavirus (HCoV)-NL63 employs angiotensin-converting enzyme 2 (ACE2) as a receptor for cellular entry. SARS-CoV infection causes robust downregulation of cellular ACE2 expression levels and it has been suggested that the SARS-CoV effect on ACE2 is involved in the severity of disease. We investigated whether cellular ACE2 downregulation occurs at optimal replication conditions of HCoV-NL63 infection. The expression of the homologue of ACE2, the ACE protein not used as a receptor by HCoV-NL63, was measured as a control. A specific decrease for ACE2 protein level was observed when HCoV-NL63 was cultured at 34 °C. Culturing the virus at the suboptimal temperature of 37 °C resulted in low replication of the virus and the effect on ACE2 expression was lost. We conclude that the decline of ACE2 expression is dependent on the efficiency of HCoV-NL63 replication, and that HCoV-NL63 and SARS-CoV both affect cellular ACE2 expression during infection.</AbstractText>
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</MeshHeading>
<MeshHeading><DescriptorName UI="D014779" MajorTopicYN="Y">Virus Replication</DescriptorName>
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<PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2012</Year>
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<PubMedPubDate PubStatus="pubmed"><Year>2012</Year>
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<ArticleIdList><ArticleId IdType="pubmed">22718567</ArticleId>
<ArticleId IdType="doi">10.1099/vir.0.043919-0</ArticleId>
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<affiliations><list><country><li>Pays-Bas</li>
<li>Pologne</li>
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<region><li>Hollande-Septentrionale</li>
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<settlement><li>Amsterdam</li>
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<orgName><li>Université d'Amsterdam</li>
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<tree><country name="Pays-Bas"><region name="Hollande-Septentrionale"><name sortKey="Dijkman, Ronald" sort="Dijkman, Ronald" uniqKey="Dijkman R" first="Ronald" last="Dijkman">Ronald Dijkman</name>
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<name sortKey="Buelow, Elena" sort="Buelow, Elena" uniqKey="Buelow E" first="Elena" last="Buelow">Elena Buelow</name>
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<name sortKey="Van Der Bijl, Anna" sort="Van Der Bijl, Anna" uniqKey="Van Der Bijl A" first="Anna" last="Van Der Bijl">Anna Van Der Bijl</name>
<name sortKey="Van Der Hoek, Lia" sort="Van Der Hoek, Lia" uniqKey="Van Der Hoek L" first="Lia" last="Van Der Hoek">Lia Van Der Hoek</name>
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<country name="Pologne"><noRegion><name sortKey="Pyrc, Krzysztof" sort="Pyrc, Krzysztof" uniqKey="Pyrc K" first="Krzysztof" last="Pyrc">Krzysztof Pyrc</name>
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