Viruses and interactomes in translation.
Identifieur interne : 000182 ( Hal/Corpus ); précédent : 000181; suivant : 000183Viruses and interactomes in translation.
Auteurs : Laurène Meyniel-Schicklin ; Benoît De Chassey ; Patrice André ; Vincent LotteauSource :
- Molecular and Cellular Proteomics [ 1535-9476 ] ; 2012-07.
Abstract
A decade of high-throughput screenings for intraviral and virus-host protein-protein interactions led to the accumulation of data and to the development of theories on laws governing interactome organization for many viruses. We present here a computational analysis of intraviral protein networks (EBV, FLUAV, HCV, HSV-1, KSHV, SARS-CoV, VACV, and VZV) and virus-host protein networks (DENV, EBV, FLUAV, HCV, and VACV) from up-to-date interaction data, using various mathematical approaches. If intraviral networks seem to behave similarly, they are clearly different from the human interactome. Viral proteins target highly central human proteins, which are precisely the Achilles' heel of the human interactome. The intrinsic structural disorder is a distinctive feature of viral hubs in virus-host interactomes. Overlaps between virus-host data sets identify a core of human proteins involved in the cellular response to viral infection and in the viral capacity to hijack the cell machinery for viral replication. Host proteins that are strongly targeted by a virus seem to be particularly attractive for other viruses. Such protein-protein interaction networks and their analysis represent a powerful resource from a therapeutic perspective.
Url:
DOI: 10.1074/mcp.M111.014738
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<front><div type="abstract" xml:lang="en"> <p>A decade of high-throughput screenings for intraviral and virus-host protein-protein interactions led to the accumulation of data and to the development of theories on laws governing interactome organization for many viruses. We present here a computational analysis of intraviral protein networks (EBV, FLUAV, HCV, HSV-1, KSHV, SARS-CoV, VACV, and VZV) and virus-host protein networks (DENV, EBV, FLUAV, HCV, and VACV) from up-to-date interaction data, using various mathematical approaches. If intraviral networks seem to behave similarly, they are clearly different from the human interactome. Viral proteins target highly central human proteins, which are precisely the Achilles' heel of the human interactome. The intrinsic structural disorder is a distinctive feature of viral hubs in virus-host interactomes. Overlaps between virus-host data sets identify a core of human proteins involved in the cellular response to viral infection and in the viral capacity to hijack the cell machinery for viral replication. Host proteins that are strongly targeted by a virus seem to be particularly attractive for other viruses. Such protein-protein interaction networks and their analysis represent a powerful resource from a therapeutic perspective.</p>
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<idno type="halRefHtml">Molecular and Cellular Proteomics, American Society for Biochemistry and Molecular Biology, 2012, 11 (7), pp.M111.014738. ⟨10.1074/mcp.M111.014738⟩</idno>
<idno type="halRef">Molecular and Cellular Proteomics, American Society for Biochemistry and Molecular Biology, 2012, 11 (7), pp.M111.014738. ⟨10.1074/mcp.M111.014738⟩</idno>
</publicationStmt>
<seriesStmt> <idno type="stamp" n="ECOFECT">ECOFECT - Dynamiques éco-évolutives des maladies infectieuses</idno>
<idno type="stamp" n="UNIV-LYON1">Université Claude Bernard - Lyon I</idno>
<idno type="stamp" n="UDL">UDL</idno>
<idno type="stamp" n="UNIV-LYON">Université de Lyon</idno>
</seriesStmt>
<notesStmt> <note type="audience" n="2">International</note>
<note type="popular" n="0">No</note>
<note type="peer" n="1">Yes</note>
</notesStmt>
<sourceDesc> <biblStruct> <analytic> <title xml:lang="en">Viruses and interactomes in translation.</title>
<author role="aut"> <persName> <forename type="first">Laurène</forename>
<surname>Meyniel-Schicklin</surname>
</persName>
<idno type="halauthorid">1003159</idno>
<affiliation ref="#struct-27478"></affiliation>
</author>
<author role="aut"> <persName> <forename type="first">Benoît</forename>
<surname>De Chassey</surname>
</persName>
<idno type="halauthorid">1003773</idno>
<affiliation ref="#struct-71042"></affiliation>
</author>
<author role="aut"> <persName> <forename type="first">Patrice</forename>
<surname>André</surname>
</persName>
<idno type="halauthorid">169560</idno>
<affiliation ref="#struct-27478"></affiliation>
<affiliation ref="#struct-301088"></affiliation>
</author>
<author role="aut"> <persName> <forename type="first">Vincent</forename>
<surname>Lotteau</surname>
</persName>
<idno type="halauthorid">147824</idno>
<affiliation ref="#struct-27478"></affiliation>
<affiliation ref="#struct-301088"></affiliation>
</author>
</analytic>
<monogr> <idno type="halJournalId" status="VALID">17152</idno>
<idno type="issn">1535-9476</idno>
<idno type="eissn">1535-9484</idno>
<title level="j">Molecular and Cellular Proteomics</title>
<imprint> <publisher>American Society for Biochemistry and Molecular Biology</publisher>
<biblScope unit="volume">11</biblScope>
<biblScope unit="issue">7</biblScope>
<biblScope unit="pp">M111.014738</biblScope>
<date type="datePub">2012-07</date>
<date type="dateEpub">2012-02-27</date>
</imprint>
</monogr>
<idno type="doi">10.1074/mcp.M111.014738</idno>
<idno type="pubmed">22371486</idno>
</biblStruct>
</sourceDesc>
<profileDesc> <langUsage> <language ident="en">English</language>
</langUsage>
<textClass> <classCode scheme="mesh">Computer Simulation</classCode>
<classCode scheme="mesh">Host-Pathogen Interactions</classCode>
<classCode scheme="mesh">Humans</classCode>
<classCode scheme="mesh">Models, Statistical</classCode>
<classCode scheme="mesh">Protein Interaction Mapping</classCode>
<classCode scheme="mesh">Protein Interaction Maps</classCode>
<classCode scheme="mesh">Viral Proteins</classCode>
<classCode scheme="mesh">Virus Replication</classCode>
<classCode scheme="mesh">Viruses</classCode>
<classCode scheme="halDomain" n="sdv">Life Sciences [q-bio]</classCode>
<classCode scheme="halTypology" n="ART">Journal articles</classCode>
</textClass>
<abstract xml:lang="en"> <p>A decade of high-throughput screenings for intraviral and virus-host protein-protein interactions led to the accumulation of data and to the development of theories on laws governing interactome organization for many viruses. We present here a computational analysis of intraviral protein networks (EBV, FLUAV, HCV, HSV-1, KSHV, SARS-CoV, VACV, and VZV) and virus-host protein networks (DENV, EBV, FLUAV, HCV, and VACV) from up-to-date interaction data, using various mathematical approaches. If intraviral networks seem to behave similarly, they are clearly different from the human interactome. Viral proteins target highly central human proteins, which are precisely the Achilles' heel of the human interactome. The intrinsic structural disorder is a distinctive feature of viral hubs in virus-host interactomes. Overlaps between virus-host data sets identify a core of human proteins involved in the cellular response to viral infection and in the viral capacity to hijack the cell machinery for viral replication. Host proteins that are strongly targeted by a virus seem to be particularly attractive for other viruses. Such protein-protein interaction networks and their analysis represent a powerful resource from a therapeutic perspective.</p>
</abstract>
</profileDesc>
</hal>
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