Antagonism of STAT1 by Nipah virus P gene products modulates disease course but not lethal outcome in the ferret model
Identifieur interne : 000A84 ( Main/Merge ); précédent : 000A83; suivant : 000A85Antagonism of STAT1 by Nipah virus P gene products modulates disease course but not lethal outcome in the ferret model
Auteurs : Benjamin A. Satterfield [États-Unis] ; Viktoriya Borisevich [États-Unis] ; Stephanie L. Foster [États-Unis] ; Sergio E. Rodriguez [États-Unis] ; Robert W. Cross [États-Unis] ; Karla A. Fenton [États-Unis] ; Krystle N. Agans [États-Unis] ; Christopher F. Basler [États-Unis] ; Thomas W. Geisbert [États-Unis] ; Chad E. Mire [États-Unis]Source :
- Scientific Reports [ 2045-2322 ] ; 2019.
Abstract
Nipah virus (NiV) is a pathogenic paramyxovirus and zoononis with very high human fatality rates. Previous protein over-expression studies have shown that various mutations to the common N-terminal STAT1-binding motif of the NiV P, V, and W proteins affected the STAT1-binding ability of these proteins thus interfering with he JAK/STAT pathway and reducing their ability to inhibit type-I IFN signaling, but due to differing techniques it was unclear which amino acids were most important in this interaction or what impact this had on pathogenesis
Url:
DOI: 10.1038/s41598-019-53037-0
PubMed: 31723221
PubMed Central: 6853903
Links toward previous steps (curation, corpus...)
- to stream Pmc, to step Corpus: 000193
- to stream Pmc, to step Curation: 000193
- to stream Pmc, to step Checkpoint: 000A10
- to stream Ncbi, to step Merge: 000C06
- to stream Ncbi, to step Curation: 000C06
- to stream Ncbi, to step Checkpoint: 000C06
Links to Exploration step
PMC:6853903Le document en format XML
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<institution>University of Texas Medical Branch,</institution>
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Galveston, TX USA</nlm:aff>
<country>États-Unis</country>
<placeName><region type="state">Texas</region>
</placeName>
<wicri:cityArea>Galveston</wicri:cityArea>
</affiliation>
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<institution-id institution-id-type="GRID">grid.176731.5</institution-id>
<institution>Department of Microbiology and Immunology,</institution>
<institution>University of Texas Medical Branch,</institution>
</institution-wrap>
Galveston, TX USA</nlm:aff>
<country>États-Unis</country>
<placeName><region type="state">Texas</region>
</placeName>
<wicri:cityArea>Galveston</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Agans, Krystle N" sort="Agans, Krystle N" uniqKey="Agans K" first="Krystle N." last="Agans">Krystle N. Agans</name>
<affiliation wicri:level="2"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 1547 9964</institution-id>
<institution-id institution-id-type="GRID">grid.176731.5</institution-id>
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Galveston, TX USA</nlm:aff>
<country>États-Unis</country>
<placeName><region type="state">Texas</region>
</placeName>
<wicri:cityArea>Galveston</wicri:cityArea>
</affiliation>
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<institution-id institution-id-type="GRID">grid.176731.5</institution-id>
<institution>Department of Microbiology and Immunology,</institution>
<institution>University of Texas Medical Branch,</institution>
</institution-wrap>
Galveston, TX USA</nlm:aff>
<country>États-Unis</country>
<placeName><region type="state">Texas</region>
</placeName>
<wicri:cityArea>Galveston</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Basler, Christopher F" sort="Basler, Christopher F" uniqKey="Basler C" first="Christopher F." last="Basler">Christopher F. Basler</name>
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<institution-id institution-id-type="GRID">grid.256304.6</institution-id>
<institution>Center for Microbial Pathogenesis,</institution>
<institution>Institute for Biomedical Sciences, Georgia State University,</institution>
</institution-wrap>
Atlanta, GA USA</nlm:aff>
<country>États-Unis</country>
<placeName><region type="state">Géorgie (États-Unis)</region>
</placeName>
<wicri:cityArea>Atlanta</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Geisbert, Thomas W" sort="Geisbert, Thomas W" uniqKey="Geisbert T" first="Thomas W." last="Geisbert">Thomas W. Geisbert</name>
<affiliation wicri:level="2"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 1547 9964</institution-id>
<institution-id institution-id-type="GRID">grid.176731.5</institution-id>
<institution>Galveston National Laboratory,</institution>
<institution>University of Texas Medical Branch,</institution>
</institution-wrap>
Galveston, TX USA</nlm:aff>
<country>États-Unis</country>
<placeName><region type="state">Texas</region>
</placeName>
<wicri:cityArea>Galveston</wicri:cityArea>
</affiliation>
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<institution-id institution-id-type="GRID">grid.176731.5</institution-id>
<institution>Department of Microbiology and Immunology,</institution>
<institution>University of Texas Medical Branch,</institution>
</institution-wrap>
Galveston, TX USA</nlm:aff>
<country>États-Unis</country>
<placeName><region type="state">Texas</region>
</placeName>
<wicri:cityArea>Galveston</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Mire, Chad E" sort="Mire, Chad E" uniqKey="Mire C" first="Chad E." last="Mire">Chad E. Mire</name>
<affiliation wicri:level="2"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 1547 9964</institution-id>
<institution-id institution-id-type="GRID">grid.176731.5</institution-id>
<institution>Galveston National Laboratory,</institution>
<institution>University of Texas Medical Branch,</institution>
</institution-wrap>
Galveston, TX USA</nlm:aff>
<country>États-Unis</country>
<placeName><region type="state">Texas</region>
</placeName>
<wicri:cityArea>Galveston</wicri:cityArea>
</affiliation>
<affiliation wicri:level="2"><nlm:aff id="Aff2"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 1547 9964</institution-id>
<institution-id institution-id-type="GRID">grid.176731.5</institution-id>
<institution>Department of Microbiology and Immunology,</institution>
<institution>University of Texas Medical Branch,</institution>
</institution-wrap>
Galveston, TX USA</nlm:aff>
<country>États-Unis</country>
<placeName><region type="state">Texas</region>
</placeName>
<wicri:cityArea>Galveston</wicri:cityArea>
</affiliation>
</author>
</analytic>
<series><title level="j">Scientific Reports</title>
<idno type="eISSN">2045-2322</idno>
<imprint><date when="2019">2019</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><p id="Par1">Nipah virus (NiV) is a pathogenic paramyxovirus and zoononis with very high human fatality rates. Previous protein over-expression studies have shown that various mutations to the common N-terminal STAT1-binding motif of the NiV P, V, and W proteins affected the STAT1-binding ability of these proteins thus interfering with he JAK/STAT pathway and reducing their ability to inhibit type-I IFN signaling, but due to differing techniques it was unclear which amino acids were most important in this interaction or what impact this had on pathogenesis <italic>in vivo</italic>
. We compared all previously described mutations in parallel and found the amino acid mutation Y116E demonstrated the greatest reduction in binding to STAT1 and the greatest reduction in interferon antagonism. A similar reduction in binding and activity was seen for a deletion of twenty amino acids constituting the described STAT1-binding domain. To investigate the contribution of this STAT1-binding motif in NiV-mediated disease, we produced rNiVs with complete deletion of the STAT1-binding motif or the Y116E mutation for ferret challenge studies (rNiV<sub>M</sub>
-STAT1<sup>blind</sup>
). Despite the reduced IFN inhibitory function, ferrets challenged with these rNiV<sub>M</sub>
-STAT1<sup>blind</sup>
mutants had a lethal, albeit altered, NiV-mediated disease course. These data, together with our previously published data, suggest that the major role of NiV P, V, and W in NiV-mediated disease in the ferret model are likely to be in the inhibition of viral recognition/innate immune signaling induction with a minor role for inhibition of IFN signaling.</p>
</div>
</front>
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