Fig. 3.

USP25-deficient mice are more susceptible to the infection with H5N1 and HSV-1. (A) Usp25^−/− mice exhibited earlier mortality and more severe weight loss after H5N1 infection than did wild-type mice. Wild-type (n = 10) and Usp25^−/− mice (n = 11) were infected with the H5N1 influenza virus (1 × 10³ EID₅₀ per mouse) and the survival and weight loss were monitored every day. (B) The expression of Ifnb, Ifna4, and Tnf was inhibited in the lungs and livers of Usp25^−/− mice after H1N1(PR8) virus challenge compared with the wild-type mice. Mice (n = 4) were infected with H1N1(PR8) and lungs and livers were collected for qPCR analysis 24 h after infection. (C and D) Usp25^−/− mice exhibited higher mortality rate and produced decreased amount of IFN-α and IL-6 cytokines after HSV-1 challenge than did the wild-type mice. Wild-type and Usp25^−/− mice (n = 5) were infected with HSV-1 (1 × 10⁶ pfu). The survival of mice was monitored every day (C). The sera were collected at 12 h after infection followed by ELISA analysis (D). (E) Usp25^−/− mice showed less Ly6C⁺ monocytes infiltration in the lungs than did wild-type mice. Wild-type and Usp25^−/− mice (n = 3) were infected with HSV-1 (2 × 10⁶ pfu). Twenty-four hours after infection, lungs from mice were isolated and subject to histological analysis. [Original magnification, × 20 (H&E) or ×40 (Ly6C).] (Scale bars, 100 μm.) Arrow heads, infiltrated Ly6C⁺ monocytes. Data are representative of two independent experiments. *P < 0.05, **P < 0.01.