Potent and selective inhibition of SARS coronavirus replication by aurintricarboxylic acid
Identifieur interne : 000E18 ( Pmc/Curation ); précédent : 000E17; suivant : 000E19Potent 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 :
- Biochemical and Biophysical Research Communications [ 0006-291X ] ; 2004.
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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<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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<pmc article-type="research-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Biochem Biophys Res Commun</journal-id>
<journal-id journal-id-type="iso-abbrev">Biochem. Biophys. Res. Commun</journal-id>
<journal-title-group><journal-title>Biochemical and Biophysical Research Communications</journal-title>
</journal-title-group>
<issn pub-type="ppub">0006-291X</issn>
<issn pub-type="epub">1090-2104</issn>
<publisher><publisher-name>Elsevier Inc.</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">15249217</article-id>
<article-id pub-id-type="pmc">7111066</article-id>
<article-id pub-id-type="publisher-id">S0006-291X(04)01224-0</article-id>
<article-id pub-id-type="doi">10.1016/j.bbrc.2004.06.076</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>Potent and selective inhibition of SARS coronavirus replication by aurintricarboxylic acid</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>He</surname>
<given-names>Runtao</given-names>
</name>
<email>runtao_he@hc-sc.gc.ca</email>
<xref rid="AFF1" ref-type="aff">a</xref>
<xref rid="AFF2" ref-type="aff">b</xref>
<xref rid="COR1" ref-type="corresp">∗</xref>
<xref rid="FN1" ref-type="fn">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Adonov</surname>
<given-names>Anton</given-names>
</name>
<xref rid="AFF1" ref-type="aff">a</xref>
<xref rid="AFF2" ref-type="aff">b</xref>
<xref rid="FN1" ref-type="fn">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Traykova-Adonova</surname>
<given-names>Maya</given-names>
</name>
<xref rid="AFF1" ref-type="aff">a</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Cao</surname>
<given-names>Jingxin</given-names>
</name>
<xref rid="AFF1" ref-type="aff">a</xref>
<xref rid="AFF2" ref-type="aff">b</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Cutts</surname>
<given-names>Todd</given-names>
</name>
<xref rid="AFF1" ref-type="aff">a</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Grudesky</surname>
<given-names>Elsie</given-names>
</name>
<xref rid="AFF1" ref-type="aff">a</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Deschambaul</surname>
<given-names>Yvon</given-names>
</name>
<xref rid="AFF1" ref-type="aff">a</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Berry</surname>
<given-names>Jody</given-names>
</name>
<xref rid="AFF1" ref-type="aff">a</xref>
<xref rid="AFF2" ref-type="aff">b</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Drebot</surname>
<given-names>Michael</given-names>
</name>
<xref rid="AFF1" ref-type="aff">a</xref>
<xref rid="AFF2" ref-type="aff">b</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Li</surname>
<given-names>Xuguang</given-names>
</name>
<xref rid="AFF3" ref-type="aff">c</xref>
</contrib>
</contrib-group>
<aff id="AFF1"><label>a</label>
National Microbiology Laboratory, Health Canada, 1015 Arlington St., Winnipeg, MB, Canada R3E 3R2</aff>
<aff id="AFF2"><label>b</label>
Department of Medical Microbiology, School of Medicine, University of Manitoba, Winnipeg, MB, Canada R3T 2N2</aff>
<aff id="AFF3"><label>c</label>
Centre for Biologics Research, Biologics and Genetic Therapies Directorate, Health Canada, Tunney’s Pasture, Ottawa, ON, Canada K1A 0K9</aff>
<author-notes><corresp id="COR1"><label>∗</label>
Corresponding author. Fax: +1-204-789-2082 <email>runtao_he@hc-sc.gc.ca</email>
</corresp>
<fn id="FN1"><label>1</label>
<p>These authors contributed equally to the project.</p>
</fn>
</author-notes>
<pub-date pub-type="pmc-release"><day>15</day>
<month>7</month>
<year>2004</year>
</pub-date>
<pmc-comment> PMC Release delay is 0 months and 0 days and was based on .</pmc-comment>
<pub-date pub-type="ppub"><day>6</day>
<month>8</month>
<year>2004</year>
</pub-date>
<pub-date pub-type="epub"><day>15</day>
<month>7</month>
<year>2004</year>
</pub-date>
<volume>320</volume>
<issue>4</issue>
<fpage>1199</fpage>
<lpage>1203</lpage>
<history><date date-type="received"><day>27</day>
<month>5</month>
<year>2004</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2004 Elsevier Inc. All rights reserved.</copyright-statement>
<copyright-year>2004</copyright-year>
<copyright-holder>Elsevier Inc.</copyright-holder>
<license><license-p>Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.</license-p>
</license>
</permissions>
<abstract><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>
</abstract>
<kwd-group><title>Keywords</title>
<kwd>SARS</kwd>
<kwd>Coronavirus, SARS-CoV</kwd>
<kwd>Aurintricarboxylic acid</kwd>
<kwd>Inhibition</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
</record>
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