HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: vir.0.015727-0v1 90/12/2990    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Kochs, G. Articles by Staeheli, P. Search for Related Content PubMed PubMed Citation Articles by Kochs, G. Articles by Staeheli, P. Agricola Articles by Kochs, G. Articles by Staeheli, P.

Strong interferon-inducing capacity of a highly virulent variant of influenza A virus strain PR8 with deletions in the NS1 gene

¹ Department of Virology, University of Freiburg, D-79008 Freiburg, Germany
² School of Medicine and Dentistry, University of Rochester, Rochester, NY 14642, USA
³ Molecular Immunology, Helmholtz Centre for Infection Research, Braunschweig, Germany
⁴ Departments of Microbiology and Medicine (Division of Infectious Diseases) and Global Health and Emerging Pathogens Institute, Mount Sinai School of Medicine, New York, NY 10029, USA

Correspondence
Georg Kochs
georg.kochs{at}uniklinik-freiburg.de

Influenza viruses lacking the interferon (IFN)-antagonistic non-structural NS1 protein are strongly attenuated. Here, we show that mutants of a highly virulent variant of A/PR/8/34 (H1N1) carrying either a complete deletion or C-terminal truncations of NS1 were far more potent inducers of IFN in infected mice than NS1 mutants derived from standard A/PR/8/34. Efficient induction of IFN correlated with successful initial virus replication in mouse lungs, indicating that the IFN response is boosted by enhanced viral activity. As the new NS1 mutants can be handled in standard biosafety laboratories, they represent convenient novel tools for studying virus-induced IFN expression in vivo.

This article has been cited by other articles:

				C. Seitz, T. Frensing, D. Hoper, G. Kochs, and U. Reichl High yields of influenza A virus in Madin-Darby canine kidney cells are promoted by an insufficient interferon-induced antiviral state J. Gen. Virol., July 1, 2010; 91(7): 1754 - 1763. [Abstract] [Full Text] [PDF]