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Article: CK2beta gene silencing increases cell susceptibility to influenza A virus infection resulting in accelerated virus entry and higher viral protein content

TitleCK2beta gene silencing increases cell susceptibility to influenza A virus infection resulting in accelerated virus entry and higher viral protein content
Authors
Issue Date2008
PublisherBioMed Central Ltd. The Journal's web site is located at http://www.jmolecularsignaling.com
Citation
Journal Of Molecular Signaling, 2008, v. 3 How to Cite?
AbstractBackground: Influenza A virus (IVA) exploits diverse cellular gene products to support its replication in the host. The significance of the regulatory (β) subunit of casein kinase 2 (CK2β) in various cellular mechanisms is well established, but less is known about its potential role in IVA replication. We studied the role of CK2β in IVA-infected A549 human epithelial lung cells. Results: Activation of CK2β was observed in A549 cells during virus binding and internalization but appeared to be constrained as replication began. We used small interfering RNAs (siRNAs) targeting CK2β mRNA to silence CK2β protein expression in A549 cells without affecting expression of the CK2α subunit. CK2β gene silencing led to increased virus titers, consistent with the inhibition of CK2β during IVA replication. Notably, virus titers increased significantly when CK2β siRNA-transfected cells were inoculated at a lower multiplicity of infection. Virus titers also increased in cells treated with a specific CK2 inhibitor but decreased in cells treated with a CK2β stimulator. CK2β absence did not impair nuclear export of viral ribonucleoprotein complexes (6 h and 8 h after inoculation) or viral polymerase activity (analyzed in a minigenome system). The enhancement of virus titers by CK2β siRNA reflects increased cell susceptibility to influenza virus infection resulting in accelerated virus entry and higher viral protein content. Conclusion: This study demonstrates the role of cellular CK2β protein in the viral biology. Our results are the first to demonstrate a functional link between siRNA-mediated inhibition of the CK2β protein and regulation of influenza A virus replication in infected cells. Overall, the data suggest that expression and activation of CK2β inhibits influenza virus replication by regulating the virus entry process and viral protein synthesis. © 2008 Marjuki et al; licensee BioMed Central Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/179813
ISSN
2015 SCImago Journal Rankings: 1.705
References

 

DC FieldValueLanguage
dc.contributor.authorMarjuki, Hen_US
dc.contributor.authorScholtissek, Cen_US
dc.contributor.authorYen, HLen_US
dc.contributor.authorWebster, RGen_US
dc.date.accessioned2012-12-19T10:05:08Z-
dc.date.available2012-12-19T10:05:08Z-
dc.date.issued2008en_US
dc.identifier.citationJournal Of Molecular Signaling, 2008, v. 3en_US
dc.identifier.issn1750-2187en_US
dc.identifier.urihttp://hdl.handle.net/10722/179813-
dc.description.abstractBackground: Influenza A virus (IVA) exploits diverse cellular gene products to support its replication in the host. The significance of the regulatory (β) subunit of casein kinase 2 (CK2β) in various cellular mechanisms is well established, but less is known about its potential role in IVA replication. We studied the role of CK2β in IVA-infected A549 human epithelial lung cells. Results: Activation of CK2β was observed in A549 cells during virus binding and internalization but appeared to be constrained as replication began. We used small interfering RNAs (siRNAs) targeting CK2β mRNA to silence CK2β protein expression in A549 cells without affecting expression of the CK2α subunit. CK2β gene silencing led to increased virus titers, consistent with the inhibition of CK2β during IVA replication. Notably, virus titers increased significantly when CK2β siRNA-transfected cells were inoculated at a lower multiplicity of infection. Virus titers also increased in cells treated with a specific CK2 inhibitor but decreased in cells treated with a CK2β stimulator. CK2β absence did not impair nuclear export of viral ribonucleoprotein complexes (6 h and 8 h after inoculation) or viral polymerase activity (analyzed in a minigenome system). The enhancement of virus titers by CK2β siRNA reflects increased cell susceptibility to influenza virus infection resulting in accelerated virus entry and higher viral protein content. Conclusion: This study demonstrates the role of cellular CK2β protein in the viral biology. Our results are the first to demonstrate a functional link between siRNA-mediated inhibition of the CK2β protein and regulation of influenza A virus replication in infected cells. Overall, the data suggest that expression and activation of CK2β inhibits influenza virus replication by regulating the virus entry process and viral protein synthesis. © 2008 Marjuki et al; licensee BioMed Central Ltd.en_US
dc.languageengen_US
dc.publisherBioMed Central Ltd. The Journal's web site is located at http://www.jmolecularsignaling.comen_US
dc.relation.ispartofJournal of Molecular Signalingen_US
dc.titleCK2beta gene silencing increases cell susceptibility to influenza A virus infection resulting in accelerated virus entry and higher viral protein contenten_US
dc.typeArticleen_US
dc.identifier.emailYen, HL: hyen@hku.hken_US
dc.identifier.authorityYen, HL=rp00304en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1186/1750-2187-3-13en_US
dc.identifier.scopuseid_2-s2.0-48849111335en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-48849111335&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume3en_US
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridMarjuki, H=14018263900en_US
dc.identifier.scopusauthoridScholtissek, C=7006002772en_US
dc.identifier.scopusauthoridYen, HL=7102476668en_US
dc.identifier.scopusauthoridWebster, RG=36048363100en_US

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