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Potent and selective inhibition of SARS coronavirus replication by aurintricarboxylic acid

Identifieur interne : 005594 ( Main/Merge ); précédent : 005593; suivant : 005595

Potent and selective inhibition of SARS coronavirus replication by aurintricarboxylic acid

Auteurs : Runtao He [Canada] ; Anton Adonov [Canada] ; Maya Traykova-Adonova [Canada] ; Jingxin Cao [Canada] ; Todd Cutts [Canada] ; Elsie Grudesky [Canada] ; Yvon Deschambaul [Canada] ; Jody Berry [Canada] ; Michael Drebot [Canada] ; Xuguang Li [Canada]

Source :

RBID : PMC:7111066

Descripteurs français

English descriptors

Abstract

The severe acute respiratory syndrome virus (SARS) is a coronavirus that instigated regional epidemics in Canada and several Asian countries in 2003. The newly identified SARS coronavirus (SARS-CoV) can be transmitted among humans and cause severe or even fatal illnesses. As preventive vaccine development takes years to complete and adverse reactions have been reported to some veterinary coronaviral vaccines, anti-viral compounds must be relentlessly pursued. In this study, we analyzed the effect of aurintricarboxylic acid (ATA) on SARS-CoV replication in cell culture, and found that ATA could drastically inhibit SARS-CoV replication, with viral production being 1000-fold less than that in the untreated control. Importantly, when compared with IFNs α and β, viral production was inhibited by more than 1000-fold as compared with the untreated control. In addition, when compared with IFNs α and β, ATA was approximately 10 times more potent than IFN α and 100 times more than interferon β at their highest concentrations reported in the literature previously. Our data indicated that ATA should be considered as a candidate anti-SARS compound for future clinical evaluation.


Url:
DOI: 10.1016/j.bbrc.2004.06.076
PubMed: 15249217
PubMed Central: 7111066

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PMC:7111066

Le document en format XML

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<term>Antiviral Agents (pharmacology)</term>
<term>Antiviral Agents (therapeutic use)</term>
<term>Aurintricarboxylic Acid (pharmacology)</term>
<term>Cell Division (drug effects)</term>
<term>Chlorocebus aethiops</term>
<term>Dose-Response Relationship, Drug</term>
<term>Reproducibility of Results</term>
<term>SARS Virus (drug effects)</term>
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<term>Antiviraux (usage thérapeutique)</term>
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<term>Relation dose-effet des médicaments</term>
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<term>Syndrome respiratoire aigu sévère (traitement médicamenteux)</term>
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<front>
<div type="abstract" xml:lang="en">
<p>The severe acute respiratory syndrome virus (SARS) is a coronavirus that instigated regional epidemics in Canada and several Asian countries in 2003. The newly identified SARS coronavirus (SARS-CoV) can be transmitted among humans and cause severe or even fatal illnesses. As preventive vaccine development takes years to complete and adverse reactions have been reported to some veterinary coronaviral vaccines, anti-viral compounds must be relentlessly pursued. In this study, we analyzed the effect of aurintricarboxylic acid (ATA) on SARS-CoV replication in cell culture, and found that ATA could drastically inhibit SARS-CoV replication, with viral production being 1000-fold less than that in the untreated control. Importantly, when compared with IFNs α and β, viral production was inhibited by more than 1000-fold as compared with the untreated control. In addition, when compared with IFNs α and β, ATA was approximately 10 times more potent than IFN α and 100 times more than interferon β at their highest concentrations reported in the literature previously. Our data indicated that ATA should be considered as a candidate anti-SARS compound for future clinical evaluation.</p>
</div>
</front>
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<name sortKey="Hunsmann, G" uniqKey="Hunsmann G">G. Hunsmann</name>
</author>
<author>
<name sortKey="Otaka, A" uniqKey="Otaka A">A. Otaka</name>
</author>
<author>
<name sortKey="Tamamura, H" uniqKey="Tamamura H">H. Tamamura</name>
</author>
<author>
<name sortKey="Fujii, N" uniqKey="Fujii N">N. Fujii</name>
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<author>
<name sortKey="Yamamoto, N" uniqKey="Yamamoto N">N. Yamamoto</name>
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<name sortKey="Mellon, W S" uniqKey="Mellon W">W.S. Mellon</name>
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<analytic>
<author>
<name sortKey="Cavanagh, D" uniqKey="Cavanagh D">D. Cavanagh</name>
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<analytic>
<author>
<name sortKey="Marshall, E" uniqKey="Marshall E">E. Marshall</name>
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<author>
<name sortKey="Enserink, M" uniqKey="Enserink M">M. Enserink</name>
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