Näytä suppeat kuvailutiedot

dc.contributor.authorMyllys, Markko
dc.contributor.authorRuokolainen, Visa
dc.contributor.authorAho, Vesa
dc.contributor.authorSmith, Elizabeth A.
dc.contributor.authorHakanen, Satu
dc.contributor.authorPeri, Piritta
dc.contributor.authorSalvetti, Anna
dc.contributor.authorTimonen, Jussi
dc.contributor.authorHukkanen, Veijo
dc.contributor.authorLarabell, Carolyn A.
dc.contributor.authorVihinen-Ranta, Maija
dc.date.accessioned2016-07-01T05:57:30Z
dc.date.available2016-07-01T05:57:30Z
dc.date.issued2016
dc.identifier.citationMyllys, M., Ruokolainen, V., Aho, V., Smith, E. A., Hakanen, S., Peri, P., Salvetti, A., Timonen, J., Hukkanen, V., Larabell, C. A., & Vihinen-Ranta, M. (2016). Herpes simplex virus 1 induces egress channels through marginalized host chromatin. <i>Scientific Reports</i>, <i>6</i>, Article 28844. <a href="https://doi.org/10.1038/srep28844" target="_blank">https://doi.org/10.1038/srep28844</a>
dc.identifier.otherCONVID_26086930
dc.identifier.otherTUTKAID_70474
dc.identifier.urihttps://jyx.jyu.fi/handle/123456789/50668
dc.description.abstractLytic infection with herpes simplex virus type 1 (HSV-1) induces profound modification of the cell nucleus including formation of a viral replication compartment and chromatin marginalization into the nuclear periphery. We used three-dimensional soft X-ray tomography, combined with cryogenic fluorescence, confocal and electron microscopy, to analyse the transformation of peripheral chromatin during HSV-1 infection. Our data showed an increased presence of low-density gaps in the marginalized chromatin at late infection. Advanced data analysis indicated the formation of virus-nucleocapsid-sized (or wider) channels extending through the compacted chromatin of the host. Importantly, confocal and electron microscopy analysis showed that these gaps frequently contained viral nucleocapsids. These results demonstrated that HSV-1 infection induces the formation of channels penetrating the compacted layer of cellular chromatin and allowing for the passage of progeny viruses to the nuclear envelope, their site of nuclear egress.
dc.language.isoeng
dc.publisherNature Publishing Group
dc.relation.ispartofseriesScientific Reports
dc.subject.otherHerpes virus
dc.subject.othernuclear organisation
dc.titleHerpes simplex virus 1 induces egress channels through marginalized host chromatin
dc.typearticle
dc.identifier.urnURN:NBN:fi:jyu-201606303413
dc.contributor.laitosBio- ja ympäristötieteiden laitosfi
dc.contributor.laitosFysiikan laitosfi
dc.contributor.laitosDepartment of Biological and Environmental Scienceen
dc.contributor.laitosDepartment of Physicsen
dc.contributor.oppiaineSolu- ja molekyylibiologiafi
dc.contributor.oppiaineFysiikkafi
dc.contributor.oppiaineNanoscience Centerfi
dc.contributor.oppiaineCell and Molecular Biologyen
dc.contributor.oppiainePhysicsen
dc.contributor.oppiaineNanoscience Centeren
dc.type.urihttp://purl.org/eprint/type/JournalArticle
dc.date.updated2016-06-30T12:15:21Z
dc.type.coarhttp://purl.org/coar/resource_type/c_2df8fbb1
dc.description.reviewstatuspeerReviewed
dc.relation.issn2045-2322
dc.relation.numberinseries0
dc.relation.volume6
dc.type.versionpublishedVersion
dc.rights.copyright© the Authors, 2016. This is an open access article published by Nature. This work is licensed under a Creative Commons Attribution 4.0 International License.
dc.rights.accesslevelopenAccessfi
dc.relation.doi10.1038/srep28844
dc.type.okmA1


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