Skip to main content
. 2022 Sep 29;1(5):100057. doi: 10.1016/j.cellin.2022.100057

Fig. 3.

Fig. 3

Trim25 attenuates RABV pathogenicity in mice. (A) Schematic diagram of the construction of rRABV, rRABV-Trim25(−), and rRABV-Trim25. (B, C) BSR (B) and N2a (C) cells were infected with rRABV, rRABV-Trim25(−), or rRABV-Trim25 at an MOI of 0.01 for 48 h, and cells were collected for measurement of the protein levels of Trim25, RABV-P, and β-actin by Western blotting. (D, E) BSR (D) and N2a (E) cells were infected with rRABV, rRABV-Trim25(−), or rRABV-Trim25 at an MOI of 0.01 for the indicated time points, and the cell culture supernatants were harvested for virus titration. (F, G) Female C57BL/6 mice (n = 10) were intramuscularly (i.m.) infected with 8 × 105 FFU rRABV, rRABV-Trim25(−), or rRABV-Trim25. The survival ratio (F) and body weight change (G) was monitored daily for 21 continuous days (mean ​± ​SD; ∗, P ​< ​0.05; survival ratio was analyzed by Log-rank test). (H) Female C57BL/6 mice (n = 3) were inoculated as in (F). At 12 d.p.i., the mouse brains were harvested, prepared as paraffin sections, and analyzed by immunohistochemical staining with antibodies against RABV-P. Scale bar, 50 μm. Statistical analysis of comparisons between groups was carried out by Student’s t-test (∗, P ​< ​0.05; ∗∗, P ​< ​0.01; ∗∗∗, P ​< ​0.001). The bar graph shows the mean ​± ​SD, n ​= ​3.