Figure 5.

The therapy effects of IFN-α1b against coxsackievirus A6 (CVA6) infection in 10-day-old suckling mice. (A) The diagram showing IFN-α1b treatment of CVA6-A infection among 10-day-old suckling mice. The infected mice (n = 5) were given IFN-α1b therapy twice after CVA6-A infection, and the infection control group mice (n = 5) were injected with an identical volume of PBS instead of IFN-α1b after CVA6-A infection. The negative control group and IFN-α1b control group mice were not infected with CVA6-A. After being treated twice with IFN-α1b, no differences were observed between the suckling mice injected with CVA6-A and IFN-α1b and the negative controls (B). The survival rates (C), clinical scores (D), and body weight change (E) were the main factors measured daily until 6 dpi. The main tissues of the infected and treatment group mice were collected to detect the viral loads by using qPCR, and posttreatment with IFN-α1b, in which the viral load was identified to be significantly lower than that of the untreated group (F). In vitro, after CVA6-W infected RD cells, IFN-α1b was suggested to inhibit CVA6-W activities via CCK-8 detection (G). *p < 0.05; **p < 0.01; ***p < 0.001, ****p < 0.0001. n.s., insignificant result. Ten-day-old suckling mice were intraperitoneally injected with a lethal dose of CVA6-A, a similar viral load of CVA6-W, as well as an identical volume of DMEM. The histopathological (H) and immunohistochemical (IHC) (I) examinations of the leg muscle tissues of the CVA6-A infected mice treated with IFN-α1b or PBS (200×). The leg muscles were made into pathological sections and then observed (H). IHC examination was performed using anti-CVA6 VP2 antibody (I).