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. Author manuscript; available in PMC: 2013 May 9.
Published in final edited form as: Nature. 2012 Mar 25;484(7395):519–523. doi: 10.1038/nature10921

Figure 1. Influenza A virus replicates to higher levels in Ifitm3−/− mice.

Figure 1

Change in body mass (a) and survival (b) of WT (•) and Ifitm3−/− (□) mice following intranasal inoculation with A/X-31 and pandemic H1N1/09 Eng/195 influenza (n>5). Absence of IFITM3 expression was verified in the Ifitm3−/− mice at all time points, but was seen to increase in WT mice (b). A/X-31 viral load in the lungs of mice (n>4) was calculated over the course of infection (c) by plaque assay. Ifitm3−/− murine embryonic fibroblasts (n=3 per condition) stably-expressing Ifitm3 (+), or the empty vector (−) were left untreated (blue), or incubated with IFN-α (red) or -γ (green), then challenged with either A/X-31 or PR/8 influenza. 12h after infection, the cells were assessed for either HA expression (PR/8), or NP expression (A/X-31) (d). Results show means ± s.d. Statistical significance was assessed by Student’s t-test (**: P < 0.01; ***: P < 0.001).