Replication-dependent downregulation of cellular angiotensin-converting enzyme 2 protein expression by human coronavirus NL63.
Identifieur interne : 002520 ( Ncbi/Curation ); précédent : 002519; suivant : 002521Replication-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
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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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