SrasV1, Main, Merge, bibRecord, 003D42

Clathrin-dependent entry of severe acute respiratory syndrome coronavirus into target cells expressing ACE2 with the cytoplasmic tail deleted

Identifieur interne : 003D42 ( Main/Merge ); précédent : 003D41; suivant : 003D43

Clathrin-dependent entry of severe acute respiratory syndrome coronavirus into target cells expressing ACE2 with the cytoplasmic tail deleted

Auteurs : Yuuki Inoue [Japon] ; Nobuyuki Tanaka [Japon] ; Yoshinori Tanaka [Japon] ; Shingo Inoue [Japon] ; Kouichi Morita [Japon] ; MIN ZHUANG [Japon] ; Toshio Hattori [Japon] ; Kazuo Sugamura [Japon]

Source :

Journal of virology [ 0022-538X ] ; 2007.

RBID : Pascal:07-0486169

Descripteurs français

Pascal (Inist)
- Coronavirus, Clathrine, Aigu, Cellule cible, Virologie.

English descriptors

KwdEn :
- Acute, Clathrin, Coronavirus, Target cell, Virology.

Abstract

The penetration of various viruses into host cells is accomplished by hijacking the host endocytosis machinery. In the case of severe acute respiratory syndrome coronavirus (SARS-CoV) infection, viral entry is reported to require a low pH in intracytoplasmic vesicles; however, little is known about how SARS-CoV invades such compartments. Here we demonstrate that SARS-CoV mainly utilizes the clathrin-mediated endocytosis pathway for its entry to target cells by using infectious SARS-CoV, as well as a SARS-CoV pseudovirus packaged in the SARS-CoV envelope. The SARS-CoV entered caveolin-1-negative HepG2 cells, and the entry was significantly inhibited by treatment with chlorpromazine, an inhibitor for clathrin-dependent endocytosis, and by small interfering RNA-mediated gene silencing for the clathrin heavy chain. Furthermore, the SARS-CoV entered COS7 cells transfected with the mutant of ACE2 with the cytoplasmic tail deleted, SARS-CoV receptor, as well as the wild-type ACE2, and their entries were significantly inhibited by treatment with chlorpromazine. In addition, ACE2 translocated into EEA1-positive early endosomes immediately after the virus attachment to ACE2. These results suggest that when SARS-CoV binds ACE2 it is internalized and penetrates early endosomes in a clathrin-dependent manner and that the cytoplasmic tail of ACE2 is not required for the penetration of SARS-CoV.

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Le document en format XML

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<series><title level="j" type="main">Journal of virology</title>
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<front><div type="abstract" xml:lang="en">The penetration of various viruses into host cells is accomplished by hijacking the host endocytosis machinery. In the case of severe acute respiratory syndrome coronavirus (SARS-CoV) infection, viral entry is reported to require a low pH in intracytoplasmic vesicles; however, little is known about how SARS-CoV invades such compartments. Here we demonstrate that SARS-CoV mainly utilizes the clathrin-mediated endocytosis pathway for its entry to target cells by using infectious SARS-CoV, as well as a SARS-CoV pseudovirus packaged in the SARS-CoV envelope. The SARS-CoV entered caveolin-1-negative HepG2 cells, and the entry was significantly inhibited by treatment with chlorpromazine, an inhibitor for clathrin-dependent endocytosis, and by small interfering RNA-mediated gene silencing for the clathrin heavy chain. Furthermore, the SARS-CoV entered COS7 cells transfected with the mutant of ACE2 with the cytoplasmic tail deleted, SARS-CoV receptor, as well as the wild-type ACE2, and their entries were significantly inhibited by treatment with chlorpromazine. In addition, ACE2 translocated into EEA1-positive early endosomes immediately after the virus attachment to ACE2. These results suggest that when SARS-CoV binds ACE2 it is internalized and penetrates early endosomes in a clathrin-dependent manner and that the cytoplasmic tail of ACE2 is not required for the penetration of SARS-CoV.</div>
</front>
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<affiliations><list><country><li>Japon</li>
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<tree><country name="Japon"><noRegion><name sortKey="Inoue, Yuuki" sort="Inoue, Yuuki" uniqKey="Inoue Y" first="Yuuki" last="Inoue">Yuuki Inoue</name>
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<name sortKey="Hattori, Toshio" sort="Hattori, Toshio" uniqKey="Hattori T" first="Toshio" last="Hattori">Toshio Hattori</name>
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<name sortKey="Min Zhuang" sort="Min Zhuang" uniqKey="Min Zhuang" last="Min Zhuang">MIN ZHUANG</name>
<name sortKey="Morita, Kouichi" sort="Morita, Kouichi" uniqKey="Morita K" first="Kouichi" last="Morita">Kouichi Morita</name>
<name sortKey="Sugamura, Kazuo" sort="Sugamura, Kazuo" uniqKey="Sugamura K" first="Kazuo" last="Sugamura">Kazuo Sugamura</name>
<name sortKey="Tanaka, Nobuyuki" sort="Tanaka, Nobuyuki" uniqKey="Tanaka N" first="Nobuyuki" last="Tanaka">Nobuyuki Tanaka</name>
<name sortKey="Tanaka, Nobuyuki" sort="Tanaka, Nobuyuki" uniqKey="Tanaka N" first="Nobuyuki" last="Tanaka">Nobuyuki Tanaka</name>
<name sortKey="Tanaka, Yoshinori" sort="Tanaka, Yoshinori" uniqKey="Tanaka Y" first="Yoshinori" last="Tanaka">Yoshinori Tanaka</name>
</country>
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Clathrin-dependent entry of severe acute respiratory syndrome coronavirus into target cells expressing ACE2 with the cytoplasmic tail deleted

Clathrin-dependent entry of severe acute respiratory syndrome coronavirus into target cells expressing ACE2 with the cytoplasmic tail deleted

Source :

Descripteurs français

English descriptors

Abstract

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

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri