Novel Inhibitors of Severe Acute Respiratory Syndrome Coronavirus Entry That Act by Three Distinct Mechanisms
Identifieur interne : 001231 ( Main/Exploration ); précédent : 001230; suivant : 001232Novel Inhibitors of Severe Acute Respiratory Syndrome Coronavirus Entry That Act by Three Distinct Mechanisms
Auteurs : Adeyemi O. Adedeji ; William Severson ; Colleen Jonsson ; Kamalendra Singh ; Susan R. Weiss ; Stefan G. SarafianosSource :
- Journal of Virology [ 0022-538X ] ; 2013.
Abstract
Severe acute respiratory syndrome (SARS) is an infectious and highly contagious disease that is caused by SARS coronavirus (SARS-CoV) and for which there are currently no approved treatments. We report the discovery and characterization of small-molecule inhibitors of SARS-CoV replication that block viral entry by three different mechanisms. The compounds were discovered by screening a chemical library of compounds for blocking of entry of HIV-1 pseudotyped with SARS-CoV surface glycoprotein S (SARS-S) but not that of HIV-1 pseudotyped with vesicular stomatitis virus surface glycoprotein G (VSV-G). Studies on their mechanisms of action revealed that the compounds act by three distinct mechanisms: (i) SSAA09E2 {
Url:
DOI: 10.1128/JVI.00998-13
PubMed: 23678171
PubMed Central: 3700180
Affiliations:
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<front><div type="abstract" xml:lang="en"><p>Severe acute respiratory syndrome (SARS) is an infectious and highly contagious disease that is caused by SARS coronavirus (SARS-CoV) and for which there are currently no approved treatments. We report the discovery and characterization of small-molecule inhibitors of SARS-CoV replication that block viral entry by three different mechanisms. The compounds were discovered by screening a chemical library of compounds for blocking of entry of HIV-1 pseudotyped with SARS-CoV surface glycoprotein S (SARS-S) but not that of HIV-1 pseudotyped with vesicular stomatitis virus surface glycoprotein G (VSV-G). Studies on their mechanisms of action revealed that the compounds act by three distinct mechanisms: (i) SSAA09E2 {<italic>N</italic>
-[[4-(4-methylpiperazin-1-yl)phenyl]methyl]-1,2-oxazole-5-carboxamide} acts through a novel mechanism of action, by blocking early interactions of SARS-S with the receptor for SARS-CoV, angiotensin converting enzyme 2 (ACE2); (ii) SSAA09E1 {[(<italic>Z</italic>
)-1-thiophen-2-ylethylideneamino]thiourea} acts later, by blocking cathepsin L, a host protease required for processing of SARS-S during viral entry; and (iii) SSAA09E3 [<italic>N</italic>
-(9,10-dioxo-9,10-dihydroanthracen-2-yl)benzamide] also acts later and does not affect interactions of SARS-S with ACE2 or the enzymatic functions of cathepsin L but prevents fusion of the viral membrane with the host cellular membrane. Our work demonstrates that there are at least three independent strategies for blocking SARS-CoV entry, validates these mechanisms of inhibition, and introduces promising leads for the development of SARS therapeutics.</p>
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<tree><noCountry><name sortKey="Adedeji, Adeyemi O" sort="Adedeji, Adeyemi O" uniqKey="Adedeji A" first="Adeyemi O." last="Adedeji">Adeyemi O. Adedeji</name>
<name sortKey="Jonsson, Colleen" sort="Jonsson, Colleen" uniqKey="Jonsson C" first="Colleen" last="Jonsson">Colleen Jonsson</name>
<name sortKey="Sarafianos, Stefan G" sort="Sarafianos, Stefan G" uniqKey="Sarafianos S" first="Stefan G." last="Sarafianos">Stefan G. Sarafianos</name>
<name sortKey="Severson, William" sort="Severson, William" uniqKey="Severson W" first="William" last="Severson">William Severson</name>
<name sortKey="Singh, Kamalendra" sort="Singh, Kamalendra" uniqKey="Singh K" first="Kamalendra" last="Singh">Kamalendra Singh</name>
<name sortKey="Weiss, Susan R" sort="Weiss, Susan R" uniqKey="Weiss S" first="Susan R." last="Weiss">Susan R. Weiss</name>
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