[Cell entry mechanisms of coronaviruses].
Identifieur interne : 002972 ( Main/Exploration ); précédent : 002971; suivant : 002973[Cell entry mechanisms of coronaviruses].
Auteurs : Fumihiro Taguchi [Japon] ; Shutoku MatsuyamaSource :
- Uirusu [ 0042-6857 ] ; 2009.
Descripteurs français
- KwdFr :
- Animaux, Antigènes CD, Coronavirus (pathogénicité), Endosomes, Fusion membranaire, Glycoprotéine de spicule des coronavirus, Glycoprotéines membranaires (physiologie), Humains, Membrane cellulaire (virologie), Molécules d'adhérence cellulaire, Peptide hydrolases (physiologie), Protéines de l'enveloppe virale (physiologie), Récepteurs viraux (physiologie), Souris.
- MESH :
- pathogénicité : Coronavirus.
- physiologie : Glycoprotéines membranaires, Peptide hydrolases, Protéines de l'enveloppe virale, Récepteurs viraux.
- virologie : Membrane cellulaire.
- Animaux, Antigènes CD, Endosomes, Fusion membranaire, Glycoprotéine de spicule des coronavirus, Humains, Molécules d'adhérence cellulaire, Souris.
English descriptors
- KwdEn :
- Animals, Antigens, CD, Cell Adhesion Molecules, Cell Membrane (virology), Coronavirus (pathogenicity), Endosomes, Humans, Membrane Fusion, Membrane Glycoproteins (physiology), Mice, Peptide Hydrolases (physiology), Receptors, Virus (physiology), Spike Glycoprotein, Coronavirus, Viral Envelope Proteins (physiology).
- MESH :
- chemical , physiology : Membrane Glycoproteins, Peptide Hydrolases, Receptors, Virus, Viral Envelope Proteins.
- chemical : Antigens, CD, Cell Adhesion Molecules, Spike Glycoprotein, Coronavirus.
- pathogenicity : Coronavirus.
- virology : Cell Membrane.
- Animals, Endosomes, Humans, Membrane Fusion, Mice.
Abstract
Enveloped viruses enter into cells via fusion of their envelope and cellular membrane. Spike (S) protein of coronavirus (CoV) is responsible for entry events. We studied the cell entry mechanisms of two different CoVs, murine coronavirus mouse hepatitis virus (MHV) and severe acute respiratory syndrome coronavirus (SARS-CoV). MHV-JHM that induces syncytia in infected cells entered directly from cell surface, i.e., fusion of envelope and plasma membrane, whereas SARS-CoV and MHV-2 that fail to induce syncytia entered via endosome in a protease-dependent fashion, i.e., fusion of envelope and endosomal membrane. The latter viruses entered directly from cell surface, when receptor-bound viruses were treated with proteases that activate fusion activity of their S proteins. The entry pathway of SARS-CoV could influence the severity of the disease. It was also reveled that a highly neurovirulent JHM spread in a receptor-independent fashion, which could result in a high neuropathogenicity of the virus.
DOI: 10.2222/jsv.59.215
PubMed: 20218330
Affiliations:
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Le document en format XML
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wicri:level="1"><nlm:affiliation>Laboratory of Virology and Viral Diseases, Faculty of Veterinary Medicine, Nippon Veterinary and Life Science University. ftaguchi@nvlu.ac.jp</nlm:affiliation><country wicri:rule="url">Japon</country></affiliation></author><author><name sortKey="Matsuyama, Shutoku" sort="Matsuyama, Shutoku" uniqKey="Matsuyama S" first="Shutoku" last="Matsuyama">Shutoku Matsuyama</name></author></analytic><series><title level="j">Uirusu</title><idno type="ISSN">0042-6857</idno><imprint><date when="2009" type="published">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antigens, CD</term><term>Cell Adhesion Molecules</term><term>Cell Membrane (virology)</term><term>Coronavirus (pathogenicity)</term><term>Endosomes</term><term>Humans</term><term>Membrane Fusion</term><term>Membrane Glycoproteins (physiology)</term><term>Mice</term><term>Peptide Hydrolases (physiology)</term><term>Receptors, Virus (physiology)</term><term>Spike Glycoprotein, Coronavirus</term><term>Viral Envelope Proteins (physiology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Antigènes CD</term><term>Coronavirus (pathogénicité)</term><term>Endosomes</term><term>Fusion membranaire</term><term>Glycoprotéine de spicule des coronavirus</term><term>Glycoprotéines membranaires (physiologie)</term><term>Humains</term><term>Membrane cellulaire (virologie)</term><term>Molécules d'adhérence cellulaire</term><term>Peptide hydrolases (physiologie)</term><term>Protéines de l'enveloppe virale (physiologie)</term><term>Récepteurs viraux (physiologie)</term><term>Souris</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Membrane Glycoproteins</term><term>Peptide Hydrolases</term><term>Receptors, Virus</term><term>Viral Envelope Proteins</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Antigens, CD</term><term>Cell Adhesion Molecules</term><term>Spike Glycoprotein, Coronavirus</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Coronavirus</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Coronavirus</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Glycoprotéines membranaires</term><term>Peptide hydrolases</term><term>Protéines de l'enveloppe virale</term><term>Récepteurs viraux</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Membrane cellulaire</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Cell Membrane</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Endosomes</term><term>Humans</term><term>Membrane Fusion</term><term>Mice</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Antigènes CD</term><term>Endosomes</term><term>Fusion membranaire</term><term>Glycoprotéine de spicule des coronavirus</term><term>Humains</term><term>Molécules d'adhérence cellulaire</term><term>Souris</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Enveloped viruses enter into cells via fusion of their envelope and cellular membrane. Spike (S) protein of coronavirus (CoV) is responsible for entry events. We studied the cell entry mechanisms of two different CoVs, murine coronavirus mouse hepatitis virus (MHV) and severe acute respiratory syndrome coronavirus (SARS-CoV). MHV-JHM that induces syncytia in infected cells entered directly from cell surface, i.e., fusion of envelope and plasma membrane, whereas SARS-CoV and MHV-2 that fail to induce syncytia entered via endosome in a protease-dependent fashion, i.e., fusion of envelope and endosomal membrane. The latter viruses entered directly from cell surface, when receptor-bound viruses were treated with proteases that activate fusion activity of their S proteins. The entry pathway of SARS-CoV could influence the severity of the disease. It was also reveled that a highly neurovirulent JHM spread in a receptor-independent fashion, which could result in a high neuropathogenicity of the virus.</div></front></TEI><affiliations><list><country><li>Japon</li></country></list><tree><noCountry><name sortKey="Matsuyama, Shutoku" sort="Matsuyama, Shutoku" uniqKey="Matsuyama S" first="Shutoku" last="Matsuyama">Shutoku Matsuyama</name></noCountry><country name="Japon"><noRegion><name sortKey="Taguchi, Fumihiro" sort="Taguchi, Fumihiro" uniqKey="Taguchi F" first="Fumihiro" last="Taguchi">Fumihiro Taguchi</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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