Figure 4

Stimulation of α2-ARs inhibits a step of the virus life cycle after protein synthesis. (A) Effect of α2-AR agonists on influenza virus replication. AX4/PB2 cells were treated with dexmedetomidine (Dex), guanfacine (Gua), rilmenidine (Ril), tizanidine (Tiz), or xyladine (Xyl), and subjected to a virus replication assay with Rluc. Data are shown as means ± SEM of three independent experiments. (B) Effect of α2-AR antagonists on clonidine-induced inhibition of virus replication. AX4/PB2 cells were treated with atipamezole (Ati), yohimbine (Yoh), or BRL-44408 (BRL) in the presence of 1 µM clonidine, and subjected to a virus replication assay with Rluc. Data are shown as means ± SEM of three independent experiments. (C) Effect of clonidine on viral protein expression. AX4/PB2 cells were infected with WSN/PB2-Rluc virus at an MOI of 1 and the remaining viruses were removed. After 6 h of treatment with 100 µM favipiravir (Fav), 1 µM zanamivir (Zan), or 10 µM clonidine (Clo), viral protein expression levels were assessed on the basis of Rluc expression levels. Data are shown as means ± SEM of three independent experiments.