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CK2 beta gene silencing increases cell susceptibility to influenza A virus infection resulting in accelerated virus entry and higher viral protein content by Henju Marjuki; Christoph Scholtissek; Hui-Ling Yen; Robert G Webster is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

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## Background 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. __CK2__β 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 pol

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Author

Henju Marjuki; Christoph Scholtissek; Hui-Ling Yen; Robert G Webster

Publisher

BioMed Central; Ubiquity Press, Ltd.; [London]: BioMed Central, c2006-; London: Ubiquity Press (ISSN 1750-2187)

Published

2008

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)