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2019-03-22Zeitschriftenartikel DOI: 10.25646/6163
Differential Innate Immune Responses Elicited by Nipah Virus and Cedar Virus Correlate with Disparate In Vivo Pathogenesis in Hamsters
dc.contributor.authorSchountz, Tony
dc.contributor.authorCampbell, Corey
dc.contributor.authorWagner, Kaitlyn
dc.contributor.authorRovnak, Joel
dc.contributor.authorMartellaro, Cynthia
dc.contributor.authorDeBuysscher, Blair L.
dc.contributor.authorFeldmann, Heinz
dc.contributor.authorPrescott, Joseph
dc.date.accessioned2019-05-28T08:59:26Z
dc.date.available2019-05-28T08:59:26Z
dc.date.issued2019-03-22none
dc.identifier.other10.3390/v11030291
dc.identifier.urihttp://edoc.rki.de/176904/6190
dc.description.abstractSyrian hamsters (Mesocricetus auratus) are a pathogenesis model for the Nipah virus (NiV), and we sought to determine if they are also susceptible to the Cedar virus (CedPV). Following intranasal inoculation with CedPV, virus replication occurred in the lungs and spleens of infected hamsters, a neutralizing antibody was produced in some hamsters within 8 days post-challenge, and no conspicuous signs of disease occurred. CedPV replicated to a similar magnitude as NiV-Bangladesh in type I IFN-deficient BHK-21 Syrian hamster fibroblasts but replicated 4 logs lower in type I IFN-competent primary Syrian hamster and human pulmonary endothelial cells, a principal target of henipaviruses. The coinfection of these cells with CedPV and NiV failed to rescue CedPV titers and did not diminish NiV titers, suggesting the replication machinery is virus-specific. Type I IFN response transcripts Ifna7, Ddx58, Stat1, Stat2, Ccl5, Cxcl10, Isg20, Irf7, and Iigp1 were all significantly elevated in CedPV-infected hamster endothelial cells, whereas Ifna7 and Iigp1 expression were significantly repressed during NiV infection. These results are consistent with the hypothesis that CedPV’s inability to counter the host type I IFN response may, in part, contribute to its lack of pathogenicity. Because NiV causes a fatal disease in Syrian hamsters with similarities to human disease, this model will provide valuable information about the pathogenic mechanisms of henipaviruses.eng
dc.language.isoengnone
dc.publisherRobert Koch-Institut
dc.rights(CC BY 3.0 DE) Namensnennung 3.0 Deutschlandger
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/de/
dc.subjectCedar viruseng
dc.subjecthenipaviruseng
dc.subjectparamyxoviruseng
dc.subjectbat viruseng
dc.subjectSyrian hamstereng
dc.subjectantiviral responseeng
dc.subject.ddc610 Medizin und Gesundheitnone
dc.titleDifferential Innate Immune Responses Elicited by Nipah Virus and Cedar Virus Correlate with Disparate In Vivo Pathogenesis in Hamstersnone
dc.typearticle
dc.identifier.urnurn:nbn:de:kobv:0257-176904/6190-0
dc.identifier.doihttp://dx.doi.org/10.25646/6163
dc.type.versionpublishedVersionnone
local.edoc.container-titleVirusesnone
local.edoc.type-nameZeitschriftenartikel
local.edoc.container-typeperiodical
local.edoc.container-type-nameZeitschrift
local.edoc.container-urlhttps://www.mdpi.com/1999-4915/11/3/291none
local.edoc.container-publisher-nameMolecular Diversity Preservation International (MDPI)none
local.edoc.container-volume11none
local.edoc.container-issue3none
local.edoc.container-reportyear2019none
local.edoc.container-year2019none
local.edoc.container-firstpage1none
local.edoc.container-lastpage11none
local.edoc.rki-departmentZentrum für Biologische Gefahren und Spezielle Pathogenenone
dc.description.versionPeer Reviewednone

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