Fig. 5: Human-origin H1N1 influenza virus adapts to a new species more readily in the absence of IFITM3.
From: Innate immune control of influenza virus interspecies adaptation via IFITM3

Influenza virus A/California/04/2009 (H1N1) was passaged through mice as described in Fig. 4a. Groups of WT mice (n = 5 per group) were challenged with 1000 TCID50 of A/California/04/2009 (H1N1) virus passaged 1, 5, or 10 times through WT or Ifitm3−/− mice and compared to the parent virus (passage 0). a, e Viral titers from lung homogenates collected at day 7 (a) or day 6 (e) post infection. Error bars represent SEM, comparisons were analyzed by one-way ANOVA followed by Tukey’s multiple comparisons test. b Weight loss for the H1N1 series 1 challenge. Error bars represent SEM, comparisons were made using the Mann-Whitney test. ELISA quantification of IL-6 (c, g) and IFNβ (d, h) levels in lung homogenates of WT and IFITM3 KO mice at day 7 (c, d) or day 6 (g, h) post infection. Error bars represent SEM and comparisons were analyzed by one-way ANOVA followed by Tukey’s multiple comparisons test. f Weight loss for the H1N1 series 2 challenge. Skull and crossbones indicate humane euthanasia of all animals infected with KO passage 10. Error bars represent SEM, comparisons were made using the Mann-Whitney test. (a, c, d, e, g, h) Each dot represents an individual mouse. b, f dots represent averages of individual mice (n = 5 per group). All numbers above the graphs represent exact p-values. Source data are provided as a Source Data file.