Inhibition of severe acute respiratory syndrome coronavirus replication in a lethal SARS-CoV BALB/c mouse model by stinging nettle lectin, Urtica dioica agglutinin
Identifieur interne : 002371 ( Main/Exploration ); précédent : 002370; suivant : 002372Inhibition of severe acute respiratory syndrome coronavirus replication in a lethal SARS-CoV BALB/c mouse model by stinging nettle lectin, Urtica dioica agglutinin
Auteurs : Yohichi Kumaki [États-Unis] ; Miles K. Wandersee [États-Unis] ; Aaron J. Smith [États-Unis] ; YANCHEN ZHOU [États-Unis] ; Graham Simmons [États-Unis] ; Nathan M. Nelson [États-Unis] ; Kevin W. Bailey [États-Unis] ; Zachary G. Vest [États-Unis] ; Joseph K.-K. Li [États-Unis] ; Paul Kay-Sheung Chan [Hong Kong] ; Donald F. Smee [États-Unis] ; Dale L. Barnard [États-Unis]Source :
- Antiviral research [ 0166-3542 ] ; 2011.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
Urtica dioica agglutinin (UDA) is a small plant monomeric lectin, 8.7 kDa in size, with an N-acetylglucosamine specificity that inhibits viruses from Nidovirales in vitro. In the current study, we first examined the efficacy of UDA on the replication of different SARS-CoV strains in Vero 76 cells. UDA inhibited virus replication in a dose-dependent manner and reduced virus yields of the Urbani strain by 90% at 1.1 ± 0.4 μg/ml in Vero 76 cells. Then, UDA was tested for efficacy in a lethal SARS-CoV-infected BALB/c mouse model. BALB/c mice were infected with two LD50 (575 PFU) of virus for 4 h before the mice were treated intraperitoneally with UDA at 20,10, 5 or 0 mg/kg/day for 4 days. Treatment with UDA at 5 mg/kg significantly protected the mice against a lethal infection with mouse-adapted SARS-CoV (p < 0.001), but did not significantly reduce virus lung titers. All virus-infected mice receiving UDA treatments were also significantly protected against weight loss (p < 0.001). UDA also effectively reduced lung pathology scores. At day 6 after virus exposure, all groups of mice receiving UDA had much lower lung weights than did the placebo-treated mice. Thus, our data suggest that UDA treatment of SARS infection in mice leads to a substantial therapeutic effect that protects mice against death and weight loss. Furthermore, the mode of action of UDA in vitro was further investigated using live SARS-CoV Urbani strain virus and retroviral particles pseudotyped with SARS-CoV spike (S). UDA specifically inhibited the replication of live SARS-CoV or SARS-CoV pseudotyped virus when added just before, but not after, adsorption. These data suggested that UDA likely inhibits SARS-CoV infection by targeting early stages of the replication cycle, namely, adsorption or penetration. In addition, we demonstrated that UDA neutralizes the virus infectivity, presumably by binding to the SARS-CoV spike (S) glycoprotein. Finally, the target molecule for the inhibition of virus replication was partially characterized. When UDA was exposed to N-acetylglucosamine and then UDA was added to cells just prior to adsorption, UDA did not inhibit the virus infection. These data support the conclusion that UDA might bind to N-acetylglucosamine-like residues present on the glycosylated envelope glycoproteins, thereby preventing virus attachment to cells.
Affiliations:
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<sZ>12 aut.</sZ>
</inist:fA14>
<country>États-Unis</country>
<placeName><region type="state">Utah</region>
</placeName>
</affiliation>
</author>
</analytic>
<series><title level="j" type="main">Antiviral research</title>
<title level="j" type="abbreviated">Antivir. res.</title>
<idno type="ISSN">0166-3542</idno>
<imprint><date when="2011">2011</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt><title level="j" type="main">Antiviral research</title>
<title level="j" type="abbreviated">Antivir. res.</title>
<idno type="ISSN">0166-3542</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Agglutinin</term>
<term>Animal</term>
<term>Animal model</term>
<term>Coronavirus</term>
<term>Inhibition</term>
<term>Intraperitoneal administration</term>
<term>Lectin</term>
<term>Mechanism of action</term>
<term>Mouse</term>
<term>Replication</term>
<term>Severe acute respiratory syndrome virus</term>
<term>Treatment</term>
<term>Urtica dioica</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Inhibition</term>
<term>Voie intrapéritonéale</term>
<term>Coronavirus</term>
<term>Réplication</term>
<term>Virus syndrome respiratoire aigu sévère</term>
<term>Modèle animal</term>
<term>Lectine</term>
<term>Urtica dioica</term>
<term>Agglutinine</term>
<term>Animal</term>
<term>Souris</term>
<term>Traitement</term>
<term>Mécanisme action</term>
<term>Forme fatale</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Urtica dioica agglutinin (UDA) is a small plant monomeric lectin, 8.7 kDa in size, with an N-acetylglucosamine specificity that inhibits viruses from Nidovirales in vitro. In the current study, we first examined the efficacy of UDA on the replication of different SARS-CoV strains in Vero 76 cells. UDA inhibited virus replication in a dose-dependent manner and reduced virus yields of the Urbani strain by 90% at 1.1 ± 0.4 μg/ml in Vero 76 cells. Then, UDA was tested for efficacy in a lethal SARS-CoV-infected BALB/c mouse model. BALB/c mice were infected with two LD<sub>50</sub>
(575 PFU) of virus for 4 h before the mice were treated intraperitoneally with UDA at 20,10, 5 or 0 mg/kg/day for 4 days. Treatment with UDA at 5 mg/kg significantly protected the mice against a lethal infection with mouse-adapted SARS-CoV (p < 0.001), but did not significantly reduce virus lung titers. All virus-infected mice receiving UDA treatments were also significantly protected against weight loss (p < 0.001). UDA also effectively reduced lung pathology scores. At day 6 after virus exposure, all groups of mice receiving UDA had much lower lung weights than did the placebo-treated mice. Thus, our data suggest that UDA treatment of SARS infection in mice leads to a substantial therapeutic effect that protects mice against death and weight loss. Furthermore, the mode of action of UDA in vitro was further investigated using live SARS-CoV Urbani strain virus and retroviral particles pseudotyped with SARS-CoV spike (S). UDA specifically inhibited the replication of live SARS-CoV or SARS-CoV pseudotyped virus when added just before, but not after, adsorption. These data suggested that UDA likely inhibits SARS-CoV infection by targeting early stages of the replication cycle, namely, adsorption or penetration. In addition, we demonstrated that UDA neutralizes the virus infectivity, presumably by binding to the SARS-CoV spike (S) glycoprotein. Finally, the target molecule for the inhibition of virus replication was partially characterized. When UDA was exposed to N-acetylglucosamine and then UDA was added to cells just prior to adsorption, UDA did not inhibit the virus infection. These data support the conclusion that UDA might bind to N-acetylglucosamine-like residues present on the glycosylated envelope glycoproteins, thereby preventing virus attachment to cells.</div>
</front>
</TEI>
<affiliations><list><country><li>Hong Kong</li>
<li>États-Unis</li>
</country>
<region><li>Californie</li>
<li>Utah</li>
</region>
<settlement><li>Sha Tin</li>
</settlement>
<orgName><li>Université chinoise de Hong Kong</li>
</orgName>
</list>
<tree><country name="États-Unis"><region name="Utah"><name sortKey="Kumaki, Yohichi" sort="Kumaki, Yohichi" uniqKey="Kumaki Y" first="Yohichi" last="Kumaki">Yohichi Kumaki</name>
</region>
<name sortKey="Bailey, Kevin W" sort="Bailey, Kevin W" uniqKey="Bailey K" first="Kevin W." last="Bailey">Kevin W. Bailey</name>
<name sortKey="Barnard, Dale L" sort="Barnard, Dale L" uniqKey="Barnard D" first="Dale L." last="Barnard">Dale L. Barnard</name>
<name sortKey="Li, Joseph K K" sort="Li, Joseph K K" uniqKey="Li J" first="Joseph K.-K." last="Li">Joseph K.-K. Li</name>
<name sortKey="Nelson, Nathan M" sort="Nelson, Nathan M" uniqKey="Nelson N" first="Nathan M." last="Nelson">Nathan M. Nelson</name>
<name sortKey="Simmons, Graham" sort="Simmons, Graham" uniqKey="Simmons G" first="Graham" last="Simmons">Graham Simmons</name>
<name sortKey="Simmons, Graham" sort="Simmons, Graham" uniqKey="Simmons G" first="Graham" last="Simmons">Graham Simmons</name>
<name sortKey="Smee, Donald F" sort="Smee, Donald F" uniqKey="Smee D" first="Donald F." last="Smee">Donald F. Smee</name>
<name sortKey="Smith, Aaron J" sort="Smith, Aaron J" uniqKey="Smith A" first="Aaron J." last="Smith">Aaron J. Smith</name>
<name sortKey="Vest, Zachary G" sort="Vest, Zachary G" uniqKey="Vest Z" first="Zachary G." last="Vest">Zachary G. Vest</name>
<name sortKey="Wandersee, Miles K" sort="Wandersee, Miles K" uniqKey="Wandersee M" first="Miles K." last="Wandersee">Miles K. Wandersee</name>
<name sortKey="Yanchen Zhou" sort="Yanchen Zhou" uniqKey="Yanchen Zhou" last="Yanchen Zhou">YANCHEN ZHOU</name>
<name sortKey="Yanchen Zhou" sort="Yanchen Zhou" uniqKey="Yanchen Zhou" last="Yanchen Zhou">YANCHEN ZHOU</name>
</country>
<country name="Hong Kong"><noRegion><name sortKey="Chan, Paul Kay Sheung" sort="Chan, Paul Kay Sheung" uniqKey="Chan P" first="Paul Kay-Sheung" last="Chan">Paul Kay-Sheung Chan</name>
</noRegion>
</country>
</tree>
</affiliations>
</record>
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