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Coronaviruses lacking exoribonuclease activity are susceptible to lethal mutagenesis: evidence for proofreading and potential therapeutics.

Identifieur interne : 000039 ( Hal/Curation ); précédent : 000038; suivant : 000040

Coronaviruses lacking exoribonuclease activity are susceptible to lethal mutagenesis: evidence for proofreading and potential therapeutics.

Auteurs : Everett Clinton Smith [États-Unis] ; Hervé Blanc [France] ; Marco Vignuzzi [France] ; Mark R. Denison [États-Unis]

Source :

RBID : Hal:pasteur-00918207

Abstract

No therapeutics or vaccines currently exist for human coronaviruses (HCoVs). The Severe Acute Respiratory Syndrome-associated coronavirus (SARS-CoV) epidemic in 2002-2003, and the recent emergence of Middle East Respiratory Syndrome coronavirus (MERS-CoV) in April 2012, emphasize the high probability of future zoonotic HCoV emergence causing severe and lethal human disease. Additionally, the resistance of SARS-CoV to ribavirin (RBV) demonstrates the need to define new targets for inhibition of CoV replication. CoVs express a 3'-to-5' exoribonuclease in nonstructural protein 14 (nsp14-ExoN) that is required for high-fidelity replication and is conserved across the CoV family. All genetic and biochemical data support the hypothesis that nsp14-ExoN has an RNA proofreading function. Thus, we hypothesized that ExoN is responsible for CoV resistance to RNA mutagens. We demonstrate that while wild-type (ExoN+) CoVs were resistant to RBV and 5-fluorouracil (5-FU), CoVs lacking ExoN activity (ExoN-) were up to 300-fold more sensitive. While the primary antiviral activity of RBV against CoVs was not mutagenesis, ExoN- CoVs treated with 5-FU demonstrated both enhanced sensitivity during multi-cycle replication, as well as decreased specific infectivity, consistent with 5-FU functioning as a mutagen. Comparison of full-genome next-generation sequencing of 5-FU treated SARS-CoV populations revealed a 16-fold increase in the number of mutations within the ExoN- population as compared to ExoN+. Ninety percent of these mutations represented A:G and U:C transitions, consistent with 5-FU incorporation during RNA synthesis. Together our results constitute direct evidence that CoV ExoN activity provides a critical proofreading function during virus replication. Furthermore, these studies identify ExoN as the first viral protein distinct from the RdRp that determines the sensitivity of RNA viruses to mutagens. Finally, our results show the importance of ExoN as a target for inhibition, and suggest that small-molecule inhibitors of ExoN activity could be potential pan-CoV therapeutics in combination with RBV or RNA mutagens.


Url:
DOI: 10.1371/journal.ppat.1003565

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<idno type="stamp" n="RIIP_PARIS">Institut Pasteur de Paris</idno>
</seriesStmt>
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<note type="audience" n="2">International</note>
<note type="popular" n="0">No</note>
<note type="peer" n="1">Yes</note>
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<analytic>
<title xml:lang="en">Coronaviruses lacking exoribonuclease activity are susceptible to lethal mutagenesis: evidence for proofreading and potential therapeutics.</title>
<author role="aut">
<persName>
<forename type="first">Everett Clinton</forename>
<surname>Smith</surname>
</persName>
<idno type="halauthorid">956508</idno>
<affiliation ref="#struct-239630"></affiliation>
<affiliation ref="#struct-239631"></affiliation>
</author>
<author role="aut">
<persName>
<forename type="first">Hervé</forename>
<surname>Blanc</surname>
</persName>
<idno type="halauthorid">639803</idno>
<affiliation ref="#struct-51797"></affiliation>
</author>
<author role="aut">
<persName>
<forename type="first">Marco</forename>
<surname>Vignuzzi</surname>
</persName>
<idno type="halauthorid">389525</idno>
<affiliation ref="#struct-51797"></affiliation>
</author>
<author role="crp">
<persName>
<forename type="first">Mark R</forename>
<surname>Denison</surname>
</persName>
<email type="md5">bebd4538bf0e129c0108ecb0610db98e</email>
<email type="domain">Vanderbilt.Edu</email>
<idno type="halauthorid">956509</idno>
<affiliation ref="#struct-239630"></affiliation>
<affiliation ref="#struct-239631"></affiliation>
<affiliation ref="#struct-239632"></affiliation>
</author>
</analytic>
<monogr>
<idno type="halJournalId" status="VALID">1959</idno>
<idno type="issn">1553-7366</idno>
<idno type="eissn">1553-7374</idno>
<title level="j">PLoS Pathogens</title>
<imprint>
<publisher>Public Library of Science</publisher>
<biblScope unit="volume">9</biblScope>
<biblScope unit="issue">8</biblScope>
<biblScope unit="pp">e1003565</biblScope>
<date type="datePub">2013-08</date>
<date type="dateEpub">2013-08-15</date>
</imprint>
</monogr>
<idno type="doi">10.1371/journal.ppat.1003565</idno>
<idno type="pubmed">23966862</idno>
</biblStruct>
</sourceDesc>
<profileDesc>
<langUsage>
<language ident="en">English</language>
</langUsage>
<textClass>
<classCode scheme="halDomain" n="sdv.mp.vir">Life Sciences [q-bio]/Microbiology and Parasitology/Virology</classCode>
<classCode scheme="halTypology" n="ART">Journal articles</classCode>
</textClass>
<abstract xml:lang="en">
<p>No therapeutics or vaccines currently exist for human coronaviruses (HCoVs). The Severe Acute Respiratory Syndrome-associated coronavirus (SARS-CoV) epidemic in 2002-2003, and the recent emergence of Middle East Respiratory Syndrome coronavirus (MERS-CoV) in April 2012, emphasize the high probability of future zoonotic HCoV emergence causing severe and lethal human disease. Additionally, the resistance of SARS-CoV to ribavirin (RBV) demonstrates the need to define new targets for inhibition of CoV replication. CoVs express a 3'-to-5' exoribonuclease in nonstructural protein 14 (nsp14-ExoN) that is required for high-fidelity replication and is conserved across the CoV family. All genetic and biochemical data support the hypothesis that nsp14-ExoN has an RNA proofreading function. Thus, we hypothesized that ExoN is responsible for CoV resistance to RNA mutagens. We demonstrate that while wild-type (ExoN+) CoVs were resistant to RBV and 5-fluorouracil (5-FU), CoVs lacking ExoN activity (ExoN-) were up to 300-fold more sensitive. While the primary antiviral activity of RBV against CoVs was not mutagenesis, ExoN- CoVs treated with 5-FU demonstrated both enhanced sensitivity during multi-cycle replication, as well as decreased specific infectivity, consistent with 5-FU functioning as a mutagen. Comparison of full-genome next-generation sequencing of 5-FU treated SARS-CoV populations revealed a 16-fold increase in the number of mutations within the ExoN- population as compared to ExoN+. Ninety percent of these mutations represented A:G and U:C transitions, consistent with 5-FU incorporation during RNA synthesis. Together our results constitute direct evidence that CoV ExoN activity provides a critical proofreading function during virus replication. Furthermore, these studies identify ExoN as the first viral protein distinct from the RdRp that determines the sensitivity of RNA viruses to mutagens. Finally, our results show the importance of ExoN as a target for inhibition, and suggest that small-molecule inhibitors of ExoN activity could be potential pan-CoV therapeutics in combination with RBV or RNA mutagens.</p>
</abstract>
</profileDesc>
</hal>
</record>

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