SrasV1, PubMed, Corpus, bibRecord, 001D01

Heptad repeat-derived peptides block protease-mediated direct entry from the cell surface of severe acute respiratory syndrome coronavirus but not entry via the endosomal pathway.

Identifieur interne : 001D01 ( PubMed/Corpus ); précédent : 001D00; suivant : 001D02

Heptad repeat-derived peptides block protease-mediated direct entry from the cell surface of severe acute respiratory syndrome coronavirus but not entry via the endosomal pathway.

Auteurs : Makoto Ujike ; Hiroki Nishikawa ; Akira Otaka ; Naoki Yamamoto ; Norio Yamamoto ; Masao Matsuoka ; Eiichi Kodama ; Nobutaka Fujii ; Fumihiro Taguchi

Source :

Journal of virology [ 1098-5514 ] ; 2008.

RBID : pubmed:17942557

English descriptors

KwdEn :
- Animals, Antiviral Agents (pharmacology), Chlorocebus aethiops, Endosomes (virology), Peptide Hydrolases (physiology), Peptides (pharmacology), SARS Virus (physiology), Vero Cells, Viral Proteins (pharmacology), Virus Internalization (drug effects).
MESH :
- chemical , pharmacology : Antiviral Agents, Peptides, Viral Proteins.
- chemical , physiology : Peptide Hydrolases.
- drug effects : Virus Internalization.
- physiology : SARS Virus.
- virology : Endosomes.
- Animals, Chlorocebus aethiops, Vero Cells.

Abstract

The peptides derived from the heptad repeat (HRP) of severe acute respiratory syndrome coronavirus (SCoV) spike protein (sHRPs) are known to inhibit SCoV infection, yet their efficacies are fairly low. Recently our research showed that some proteases facilitated SCoV's direct entry from the cell surface, resulting in a more efficient infection than the previously known infection via endosomal entry. To compare the inhibitory effect of the sHRP in each pathway, we selected two sHRPs, which showed a strong inhibitory effect on the interaction of two heptad repeats in a rapid and virus-free in vitro assay system. We found that they efficiently inhibited SCoV infection of the protease-mediated cell surface pathway but had little effect on the endosomal pathway. This finding suggests that sHRPs may effectively prevent infection in the lungs, where SCoV infection could be enhanced by proteases produced in this organ. This is the first observation that HRP exhibits different effects on virus that takes the endosomal pathway and virus that enters directly from the cell surface.

DOI: 10.1128/JVI.01697-07
PubMed: 17942557

Links to Exploration step

pubmed:17942557

Le document en format XML

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<front><div type="abstract" xml:lang="en">The peptides derived from the heptad repeat (HRP) of severe acute respiratory syndrome coronavirus (SCoV) spike protein (sHRPs) are known to inhibit SCoV infection, yet their efficacies are fairly low. Recently our research showed that some proteases facilitated SCoV's direct entry from the cell surface, resulting in a more efficient infection than the previously known infection via endosomal entry. To compare the inhibitory effect of the sHRP in each pathway, we selected two sHRPs, which showed a strong inhibitory effect on the interaction of two heptad repeats in a rapid and virus-free in vitro assay system. We found that they efficiently inhibited SCoV infection of the protease-mediated cell surface pathway but had little effect on the endosomal pathway. This finding suggests that sHRPs may effectively prevent infection in the lungs, where SCoV infection could be enhanced by proteases produced in this organ. This is the first observation that HRP exhibits different effects on virus that takes the endosomal pathway and virus that enters directly from the cell surface.</div>
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   |texte=   Heptad repeat-derived peptides block protease-mediated direct entry from the cell surface of severe acute respiratory syndrome coronavirus but not entry via the endosomal pathway.
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	Serveur d'exploration SRAS
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Heptad repeat-derived peptides block protease-mediated direct entry from the cell surface of severe acute respiratory syndrome coronavirus but not entry via the endosomal pathway.

Heptad repeat-derived peptides block protease-mediated direct entry from the cell surface of severe acute respiratory syndrome coronavirus but not entry via the endosomal pathway.

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