Figure 7A showed that the phosphorylation level of IGF1R increased gradually following PR8 infection, peaked at day 7 post-infection, and then decreased slightly on day 9, which was consistent with the changes in the trend of IGF1 protein expression (Figure 3B). Figures 7B–D showed that the PI3K/AKT and MAPK signaling pathways were activated following PR8 infection; p-AKT expression was upregulated in the PI3K/AKT signaling pathway; and p-p38 and p-JNK expression were upregulated in the MAPK signaling pathway. Here, IGF1 is linked to infection.