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Article: H7N9 influenza A virus exhibits importin-α7–mediated replication in the mammalian respiratory tract

TitleH7N9 influenza A virus exhibits importin-α7–mediated replication in the mammalian respiratory tract
Authors
Issue Date2017
PublisherElsevier Inc.. The Journal's web site is located at http://ajp.amjpathol.org/
Citation
The American Journal of Pathology, 2017, v. 187 n. 4, p. 831-840 How to Cite?
AbstractThe acute respiratory distress syndrome (ARDS) is the leading cause of death in influenza A virus (IAV)-infected patients. Hereby, the cellular importin-α7 gene plays a major role. It promotes viral replication in the lung, thereby increasing the risk for the development of pneumonia complicated by ARDS. Herein, we analyzed whether the recently emerged H7N9 avian IAV has already adapted to human importin-α7 use, which is associated with high-level virus replication in the mammalian lung. Using a cell-based viral polymerase activity assay, we could detect a decreased H7N9 IAV polymerase activity when importin-α7 was silenced by siRNA. Moreover, virus replication was diminished in the murine cells lacking the importin-α7 gene. Consistently, importin-α7 knockout mice presented reduced pulmonary virus titers and lung lesions as well as enhanced survival rates compared to wild-type mice. In summary, our results show that H7N9 IAV have acquired distinct features of adaptation to human host factors that enable enhanced virulence in mammals. In particular, adaptation to human importin-α7 mediates elevated virus replication in the mammalian lung, which might have contributed to ARDS observed in H7N9-infected patients.
Persistent Identifierhttp://hdl.handle.net/10722/240195
ISSN
2017 Impact Factor: 4.069
2015 SCImago Journal Rankings: 2.653
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorBertram, S-
dc.contributor.authorThiele, S-
dc.contributor.authorDreier, C-
dc.contributor.authorResa-Infante, P-
dc.contributor.authorPreuß, A-
dc.contributor.authorvan Riel, D-
dc.contributor.authorMok, KP-
dc.contributor.authorSchwalm, F-
dc.contributor.authorPeiris, JSM-
dc.contributor.authorKlenk, HD-
dc.contributor.authorGabriel, G-
dc.date.accessioned2017-04-19T08:21:00Z-
dc.date.available2017-04-19T08:21:00Z-
dc.date.issued2017-
dc.identifier.citationThe American Journal of Pathology, 2017, v. 187 n. 4, p. 831-840-
dc.identifier.issn0002-9440-
dc.identifier.urihttp://hdl.handle.net/10722/240195-
dc.description.abstractThe acute respiratory distress syndrome (ARDS) is the leading cause of death in influenza A virus (IAV)-infected patients. Hereby, the cellular importin-α7 gene plays a major role. It promotes viral replication in the lung, thereby increasing the risk for the development of pneumonia complicated by ARDS. Herein, we analyzed whether the recently emerged H7N9 avian IAV has already adapted to human importin-α7 use, which is associated with high-level virus replication in the mammalian lung. Using a cell-based viral polymerase activity assay, we could detect a decreased H7N9 IAV polymerase activity when importin-α7 was silenced by siRNA. Moreover, virus replication was diminished in the murine cells lacking the importin-α7 gene. Consistently, importin-α7 knockout mice presented reduced pulmonary virus titers and lung lesions as well as enhanced survival rates compared to wild-type mice. In summary, our results show that H7N9 IAV have acquired distinct features of adaptation to human host factors that enable enhanced virulence in mammals. In particular, adaptation to human importin-α7 mediates elevated virus replication in the mammalian lung, which might have contributed to ARDS observed in H7N9-infected patients.-
dc.languageeng-
dc.publisherElsevier Inc.. The Journal's web site is located at http://ajp.amjpathol.org/-
dc.relation.ispartofThe American Journal of Pathology-
dc.rightsPosting accepted manuscript (postprint): © <year>. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/-
dc.titleH7N9 influenza A virus exhibits importin-α7–mediated replication in the mammalian respiratory tract-
dc.typeArticle-
dc.identifier.emailMok, KP: ch02mkp@hkucc.hku.hk-
dc.identifier.emailPeiris, JSM: malik@hkucc.hku.hk-
dc.identifier.authorityMok, KP=rp01805-
dc.identifier.authorityPeiris, JSM=rp00410-
dc.identifier.doi10.1016/j.ajpath.2016.12.017-
dc.identifier.hkuros271856-
dc.identifier.volume187-
dc.identifier.issue4-
dc.identifier.spage831-
dc.identifier.epage840-
dc.identifier.isiWOS:000398247600013-
dc.publisher.placeUnited States-

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