Interferon resistance promotes oncolysis by influenza virus NS1-deletion mutants

Thomas Muster, Julia Rajtarova, Monika Sachet, Hermann Unger, Reinhard Fleischhacker, Ingrid Romirer, Andreas Grassauer, Angelika Url, Adolfo García-Sastre, Klaus Wolff, Hubert Pehamberger, Michael Bergmann

Research output: Contribution to journalArticlepeer-review

52 Scopus citations


NS1 protein of influenza virus is a virulence factor that counteracts Type I interferon (IFN)-mediated antiviral response by the host. A recombinant influenza A virus that lacks the NS1 protein only replicates efficiently in systems that contain defective IFN pathways. We demonstrate that the conditional replication properties of NS1-modified influenza A virus mutants can be exploited for the virus-mediated oncolysis of IFN-resistant tumor cells. IFN resistance in analyzed tumor cell lines correlated with a reduced expression of STAT1. Addition of exogenous IFNα or supernatant of virus-infected endothelial cells inhibited viral oncolysis in IFN-sensitive but not in IFN-resistant cell lines. The oncolytic potential of NS1-modified influenza A virus mutants could be exploited in vivo in a SCID mouse model of a subcutaneously-implanted human IFN-resistant melanoma. The data indicate that IFN-resistant tumors are a suitable target for oncolysis induced by NS1-modified influenza virus mutants. STAT1 might serve as a marker to identify these IFN-resistant tumors.

Original languageEnglish
Pages (from-to)15-21
Number of pages7
JournalInternational Journal of Cancer
Issue number1
StatePublished - 20 May 2004


  • Conditionally-replicating-virus
  • SCID
  • STAT1


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