Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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A single N66S mutation in the PB1-F2 protein of influenza A virus increases virulence by inhibiting the early interferon response in vivo

ABSTRACT: This study used virological, histological, and global gene expression from an experimental murine model of influenza infection to study the contribution of a specific mutation in the PB1-F2 protein (PB1-F2 N66S) of influenza A to viral pathogenesis. 6-8 week old, wild-type, female, C57Bl/6 mice were inoculated individually with 30 μl (10^4 PFU) of virus (recombinant influenza A/WSN/33 carrying the PB1 gene segment from A/Hong Kong/156/97 (H5N1) or a PB1 mutant recombinant virus resulting in an amino acid change at position 66 in the PB1-F2 protein [N66S]) in phosphate-buffered saline (PBS) containing penicillin-streptomycin and bovine serum albumin (PBS-BA-PS). A total of 10^4 PFU of virus was given in all inoculations. Control mice were given PBS-BA-PS. Lung samples were taken for microarray analysis at 12h, 1d, 3d, and 5d post-infection (n=3 animals per group at each time point for virus infected animals; n=2 animals per time point for mock-infected animals).

ORGANISM(S): Mus musculus

SUBMITTER: Michael Katze

PROVIDER: E-GEOD-35940 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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A single N66S mutation in the PB1-F2 protein of influenza A virus increases virulence by inhibiting the early interferon response in vivo

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