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dc.contributor.authorShim, Jung Min
dc.contributor.authorKim, Jinhee
dc.contributor.authorTenson, Tanel
dc.contributor.authorMin, Ji-Young
dc.contributor.authorKainov, Denis
dc.date.accessioned2018-06-28T11:07:35Z
dc.date.available2018-06-28T11:07:35Z
dc.date.created2017-11-03T13:18:40Z
dc.date.issued2017
dc.identifier.citationViruses. 2017, 9(8).nb_NO
dc.identifier.issn1999-4915
dc.identifier.urihttp://hdl.handle.net/11250/2503562
dc.description.abstractHuman influenza A viruses (IAVs) cause global pandemics and epidemics, which remain serious threats to public health because of the shortage of effective means of control. To combat the surge of viral outbreaks, new treatments are urgently needed. Developing new virus control modalities requires better understanding of virus-host interactions. Here, we describe how IAV infection triggers cellular apoptosis and how this process can be exploited towards the development of new therapeutics, which might be more effective than the currently available anti-influenza drugs.nb_NO
dc.language.isoengnb_NO
dc.publisherMDPI AGnb_NO
dc.rightsNavngivelse 4.0 Internasjonal*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/deed.no*
dc.titleInfluenza virus infection, interferon response, viral counter-response, and apoptosisnb_NO
dc.typeJournal articlenb_NO
dc.typePeer reviewednb_NO
dc.description.versionpublishedVersionnb_NO
dc.source.volume9nb_NO
dc.source.journalVirusesnb_NO
dc.source.issue8nb_NO
dc.identifier.doi10.3390/v9080223
dc.identifier.cristin1510750
dc.description.localcode© 2017 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).nb_NO
cristin.unitcode194,65,15,0
cristin.unitnameInstitutt for klinisk og molekylær medisin
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1


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Navngivelse 4.0 Internasjonal
Except where otherwise noted, this item's license is described as Navngivelse 4.0 Internasjonal