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 : 002120 ( Main/Merge ); précédent : 002119; suivant : 002121Inhibition 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 ; Aaron J. Smith ; Yanchen Zhou ; Graham Simmons ; Nathan M. Nelson ; Kevin W. Bailey ; Zachary G. Vest ; Joseph K-K Li ; Paul Kay-Sheung Chan ; Donald F. Smee ; Dale L. BarnardSource :
- Antiviral research [ 1872-9096 ] ; 2011.
Descripteurs français
- KwdFr :
- Analyse de survie, Animaux, Antiviraux (administration et posologie), Cellules Vero, Femelle, Injections musculaires, Lectines végétales (administration et posologie), Maladies des rongeurs (anatomopathologie), Maladies des rongeurs (mortalité), Maladies des rongeurs (traitement médicamenteux), Maladies des rongeurs (virologie), Modèles animaux de maladie humaine, Poids du corps, Réplication virale (), Souris, Souris de lignée BALB C, Syndrome respiratoire aigu sévère (anatomopathologie), Syndrome respiratoire aigu sévère (mortalité), Syndrome respiratoire aigu sévère (traitement médicamenteux), Syndrome respiratoire aigu sévère (virologie), Virus du SRAS ().
- MESH :
- administration et posologie : Antiviraux, Lectines végétales.
- anatomopathologie : Maladies des rongeurs, Syndrome respiratoire aigu sévère.
- mortalité : Maladies des rongeurs, Syndrome respiratoire aigu sévère.
- traitement médicamenteux : Maladies des rongeurs, Syndrome respiratoire aigu sévère.
- virologie : Maladies des rongeurs, Syndrome respiratoire aigu sévère.
- Analyse de survie, Animaux, Cellules Vero, Femelle, Injections musculaires, Modèles animaux de maladie humaine, Poids du corps, Réplication virale, Souris, Souris de lignée BALB C, Virus du SRAS.
English descriptors
- KwdEn :
- Animals, Antiviral Agents (administration & dosage), Body Weight, Chlorocebus aethiops, Disease Models, Animal, Female, Injections, Intramuscular, Mice, Mice, Inbred BALB C, Plant Lectins (administration & dosage), Rodent Diseases (drug therapy), Rodent Diseases (mortality), Rodent Diseases (pathology), Rodent Diseases (virology), SARS Virus (drug effects), Severe Acute Respiratory Syndrome (drug therapy), Severe Acute Respiratory Syndrome (mortality), Severe Acute Respiratory Syndrome (pathology), Severe Acute Respiratory Syndrome (virology), Survival Analysis, Vero Cells, Virus Replication (drug effects).
- MESH :
- chemical , administration & dosage : Antiviral Agents, Plant Lectins.
- drug effects : SARS Virus, Virus Replication.
- drug therapy : Rodent Diseases, Severe Acute Respiratory Syndrome.
- mortality : Rodent Diseases, Severe Acute Respiratory Syndrome.
- pathology : Rodent Diseases, Severe Acute Respiratory Syndrome.
- virology : Rodent Diseases, Severe Acute Respiratory Syndrome.
- Animals, Body Weight, Chlorocebus aethiops, Disease Models, Animal, Female, Injections, Intramuscular, Mice, Mice, Inbred BALB C, Survival Analysis, Vero Cells.
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.
DOI: 10.1016/j.antiviral.2011.02.003
PubMed: 21338626
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pubmed:21338626Le document en format XML
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<term>Antiviral Agents (administration & dosage)</term>
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<term>Chlorocebus aethiops</term>
<term>Disease Models, Animal</term>
<term>Female</term>
<term>Injections, Intramuscular</term>
<term>Mice</term>
<term>Mice, Inbred BALB C</term>
<term>Plant Lectins (administration & dosage)</term>
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<term>Rodent Diseases (pathology)</term>
<term>Rodent Diseases (virology)</term>
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<term>Severe Acute Respiratory Syndrome (drug therapy)</term>
<term>Severe Acute Respiratory Syndrome (mortality)</term>
<term>Severe Acute Respiratory Syndrome (pathology)</term>
<term>Severe Acute Respiratory Syndrome (virology)</term>
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<term>Virus Replication (drug effects)</term>
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<term>Femelle</term>
<term>Injections musculaires</term>
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<term>Maladies des rongeurs (traitement médicamenteux)</term>
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<term>Lectines végétales</term>
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<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 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.</div>
</front>
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