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. 2014 Aug 12;5(11):878–882. doi: 10.1007/s13238-014-0084-6

Figure 1.

Figure 1

Virus virulence, cytokine induction and phylogenetic analyses of Guangdong H7N9 virus. (A) Weight changes of mice; (B) Mortality of mice; (C) Virus titers of the mouse lungs: five-week-old SPF BALB/c mice (seventeen mice/group) were inoculated intranasally with 106 EID50 of each virus and three mice were euthanized on 3, 5 and 7 days post-infection and lung tissues were collected for virus titration in eggs. Groups of eight BALB/c mice were monitored daily for 14 days. Data shown are the log10 geometric mean EID50/mL ± SEM. (D–J) Cytokine IP-10, TNF-α, MIP-1α, KC, MCP-1, MCP-3 and RANTES levels from virus-infected lungs were measured at days 3, and 5 dpi by ELISA. Results from each time point are expressed as mean ± SEM of three infected mice (n = 3). * P < 0.05 and ** P < 0.01. (K) Maximum likelihood phylogenies of the PA gene of the new H7N9 isolates. Branches for H7N9 were in magenta and branches for H9N2 were in black. The Guangdong H7N9 viruses from poultry and the H7N9 virus of the new influenza season were also labeled. The clades of the phylogenetic tree were classified according to the branch length and bootstrap value