Giuseppe
Emeritus
J Gen Virol. 2009 Sep 2. [Epub ahead of print]
Strong interferon-inducing capacity of a highly virulent variant of influenza A virus strain PR8 with deletions in the NS1 gene.
Kochs G, Martinez-Sobrido L, Lienenklaus S, Weiss S, Garcia-Sastre A, Staeheli P. - University of Freiburg;
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 viral replication in mouse lungs, indicating that the IFN response is boosted by enhanced viral activity. Since the new NS1 mutants can be handled in standard bio-safety laboratories, they represent convenient novel tools for studying virus-induced IFN expression in vivo.
PMID: 19726611 [PubMed - as supplied by publisher]
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Strong interferon-inducing capacity of a highly virulent variant of influenza A virus strain PR8 with deletions in the NS1 gene.
Kochs G, Martinez-Sobrido L, Lienenklaus S, Weiss S, Garcia-Sastre A, Staeheli P. - University of Freiburg;
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 viral replication in mouse lungs, indicating that the IFN response is boosted by enhanced viral activity. Since the new NS1 mutants can be handled in standard bio-safety laboratories, they represent convenient novel tools for studying virus-induced IFN expression in vivo.
PMID: 19726611 [PubMed - as supplied by publisher]
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