SrasV1, Main, Exploration, bibRecord, 002917

TACE antagonists blocking ACE2 shedding caused by the spike protein of SARS-CoV are candidate antiviral compounds

Identifieur interne : 002917 ( Main/Exploration ); précédent : 002916; suivant : 002918

TACE antagonists blocking ACE2 shedding caused by the spike protein of SARS-CoV are candidate antiviral compounds

Auteurs : Shiori Haga [Japon] ; Noriyo Nagata [Japon] ; Tadashi Okamura [Japon] ; Norio Yamamoto [Japon] ; Tetsutaro Sata [Japon] ; Naoki Yamamoto [Japon] ; Takehiko Sasazuki [Japon] ; Yukihito Ishizaka [Japon]

Source :

Antiviral research [ 0166-3542 ] ; 2010.

RBID : Pascal:10-0178272

Descripteurs français

Pascal (Inist)
- Antagoniste, Dissémination, Protéine, Virus syndrome respiratoire aigu sévère, Antiviral, Syndrome respiratoire aigu sévère, In vitro, In vivo, Pénétration virus, ADAM17.

English descriptors

KwdEn :
- ADAM17, Antagonist, Antiviral, Dissemination, In vitro, In vivo, Protein, Severe acute respiratory syndrome, Severe acute respiratory syndrome virus, Virus penetration.

Abstract

Because outbreaks of severe acute respiratory syndrome coronavirus (SARS-CoV) might reemerge, identifying antiviral compounds is of key importance. Previously, we showed that the cellular factor TNF-α converting enzyme (TACE), activated by the spike protein of SARS-CoV (SARS-S protein), was positively involved in viral entry, implying that TACE is a possible target for developing antiviral compounds. To demonstrate this possibility, we here tested the effects of TACE inhibitors on viral entry. In vitro and in vivo data revealed that the TACE inhibitor TAPI-2 attenuated entry of both pseudotyped virus expressing the SARS-S protein in a lentiviral vector backbone and infectious SARS-CoV. TAPI-2 blocked both the SARS-S protein-induced shedding of angiotensin-converting enzyme 2 (ACE2), a receptor of SARS-CoV, and TNF-α production in lung tissues. Since the downregulation of ACE2 by SARS-S protein was proposed as an etiological event in the severe clinical manifestations, our data suggest that TACE antagonists block SARS-CoV infection and also attenuate its severe clinical outcome.

Affiliations:

Links toward previous steps (curation, corpus...)

to stream PascalFrancis, to step Corpus: 000167
to stream PascalFrancis, to step Curation: 000821
to stream PascalFrancis, to step Checkpoint: 000125
to stream Main, to step Merge: 002957
to stream Main, to step Curation: 002917

Le document en format XML

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<front><div type="abstract" xml:lang="en">Because outbreaks of severe acute respiratory syndrome coronavirus (SARS-CoV) might reemerge, identifying antiviral compounds is of key importance. Previously, we showed that the cellular factor TNF-α converting enzyme (TACE), activated by the spike protein of SARS-CoV (SARS-S protein), was positively involved in viral entry, implying that TACE is a possible target for developing antiviral compounds. To demonstrate this possibility, we here tested the effects of TACE inhibitors on viral entry. In vitro and in vivo data revealed that the TACE inhibitor TAPI-2 attenuated entry of both pseudotyped virus expressing the SARS-S protein in a lentiviral vector backbone and infectious SARS-CoV. TAPI-2 blocked both the SARS-S protein-induced shedding of angiotensin-converting enzyme 2 (ACE2), a receptor of SARS-CoV, and TNF-α production in lung tissues. Since the downregulation of ACE2 by SARS-S protein was proposed as an etiological event in the severe clinical manifestations, our data suggest that TACE antagonists block SARS-CoV infection and also attenuate its severe clinical outcome.</div>
</front>
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TACE antagonists blocking ACE2 shedding caused by the spike protein of SARS-CoV are candidate antiviral compounds

TACE antagonists blocking ACE2 shedding caused by the spike protein of SARS-CoV are candidate antiviral compounds

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri