RNA-seq influenza infected B6 & D2 mice. Mus musculus

The host response to influenza A infections is strongly influenced by host genetic factors. Animal models of genetically diverse mouse strains are well suitable to identify host genes involved in severe pathology, viral replication and immune responses. Here, we have utilizing a dual RNAseq approach that allowed us to investigate both viral and host gene expression in the same individual from a single expression assay after H1N1 infection. We performed a comparative expression analysis to identify (i) correlations between host genes and the viral gene expression, (ii) host genes involved in viral replication, and (iii) genes showing differential expression between the two mouse strains after infection. These genes may be key players involved in regulating the differences in pathogenesis and host defense mechanisms after influenza A infections. Expression levels of influenza segments correlated well with the viral load and may thus be used as surrogates for conventional viral load measurements. Furthermore, we investigated the functional role of two genes, Reg3g and Irf7, in knock-out mice and found that deletion of the Irf7 gene renders the host highly susceptible to H1N1 infection. Overall design: Female, 10-12 weeks old mice were anesthetized by intra-peritoneal injection with Ketamine/Xylazine (85% NaCl (0.9%), 10% Ketamine, 5% Xylazine) with doses adjusted to the individual body weight. Mice were then intra-nasally infected with 20µl virus solution (2x10³ FFU PR8M) or mock-treated with PBS.