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  High yields of Influenza A virus in MDCK cells are promoted by an insufficient IFN-induced antiviral state

Seitz, C., Frensing, T., Höper, D., Kochs, G., & Reichl, U. (2010). High yields of Influenza A virus in MDCK cells are promoted by an insufficient IFN-induced antiviral state. Journal of General Virology, 91(7), 1754-1763. doi:10.1099/vir.0.020370-0.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0013-90B6-A Version Permalink: http://hdl.handle.net/11858/00-001M-0000-0014-A5AE-A
Genre: Journal Article

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 Creators:
Seitz, C.1, Author              
Frensing, T.1, Author              
Höper, D.2, Author
Kochs, G.3, Author
Reichl, U.1, 4, Author              
Affiliations:
1Bioprocess Engineering, Max Planck Institute for Dynamics of Complex Technical Systems, Max Planck Society, ou_1738140              
2Friedrich-Loeffler-Institut (FLI),Insel Riems, Germany, ou_persistent22              
3University of Freiburg,Department of Virology, Freiburg, GermanyFriedrich-Loeffler-Institut (FLI),Insel Riems, GermanyUniversity of Freiburg,Department of Virology, Freiburg, Germany, ou_persistent22              
4Otto-von-Guericke-Universität Magdeburg, ou_1738156              

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 Abstract: Because of their high susceptibility to infection with various influenza virus strains, Madin Darby canine kidney (MDCK) cells have been widely used as a substrate for influenza virus isolation and vaccine production. However, MDCK cells are also interferon competent and the type I interferon (IFN) response is commonly thought to be a factor strongly inhibiting virus replication. Therefore, the inhibition of influenza virus replication by IFN signalling was analysed for an adherent MDCK cell line used in vaccine manufacturing. Depending on the respective virus strain different levels of IFN induction and a corresponding up-regulation of the IFN induced myxovirus resistance protein 1 (Mx1) were observed. Suppression of IFN induction by transient expression of the viral NS1 protein enhanced replication of an influenza virus lacking NS1, but not wild type strains. In agreement with this, stimulation of cells with MDCK cell-derived IFN prior to infection resulted only in a decrease of replication rate, but not in a change of final yields for wild type influenza viruses. This lack of IFN-induced antiviral activity correlated with missing anti-influenza activity of MDCK Mx proteins. No inhibitory effect on viral polymerase activity was found for canine Mx1 and Mx2 in minireplicon assays. In conclusion, in MDCK cells IFN expression is not a limiting factor for influenza virus replication and this might be caused partially by a lack of anti-influenza activity of canine Mx proteins. Copyright © 2010 by the Society for General Microbiology. [accessed September 21st, 2010]

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Language(s): eng - English
 Dates: 2010
 Publication Status: Published in print
 Pages: -
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 Table of Contents: -
 Rev. Method: Peer
 Identifiers: eDoc: 494479
Other: 26/10
DOI: 10.1099/vir.0.020370-0
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Title: Journal of General Virology
Source Genre: Journal
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Publ. Info: London [etc.] : Society for General Microbiology [etc.]
Pages: - Volume / Issue: 91 (7) Sequence Number: - Start / End Page: 1754 - 1763 Identifier: ISSN: 0022-1317
CoNE: /journals/resource/954925413897