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

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http://pubman.mpdl.mpg.de/cone/persons/resource/persons86479

Seitz,  C.
Bioprocess Engineering, Max Planck Institute for Dynamics of Complex Technical Systems, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons86291

Frensing,  T.
Bioprocess Engineering, Max Planck Institute for Dynamics of Complex Technical Systems, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons86448

Reichl,  U.
Otto-von-Guericke-Universität Magdeburg;
Bioprocess Engineering, Max Planck Institute for Dynamics of Complex Technical Systems, Max Planck Society;

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Citation

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.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0013-90B6-A
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]