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. Author manuscript; available in PMC: 2019 Jul 1.
Published in final edited form as: J Immunol. 2018 May 16;201(1):183–192. doi: 10.4049/jimmunol.1701569

Figure 4. TRIM29 plays an important role in host defense against RNA virus infection in vivo.

Figure 4

(A) Survival of wildtype (WT) and Trim29-knockout (KO) mice (n=8 per strain) after intraperitoneal injection of reovirus (2×107 plaque-forming units (PFU) per mouse). (B) The wild-type (TRIM29+/+) and Trim29-deficient (TRIM29−/−) mice were inoculated intraperitoneally with 1×107 PFU of reovirus (Reovirus type 3 strain Dearing, T3D). At days 2 (D2) and 4 (D4) post-inoculation, mice were euthanized, and hearts were excised, frozen at −80°C, thawed, and homogenized in PBS. Levels of IFN-β in heart homogenates was quantified by ELISA. (C) The wild-type (WT, +/+) and Trim29-deficient (KO, −/−) mice were inoculated intraperitoneally with 1×107 PFU of reovirus. At day 2 (D2) and day 4 (D4) post-inoculation, mice were euthanized, intestine, spleen, liver, heart, and brain were excised, and viral titers in organ homogenates were determined by plaque assay. Results are expressed as mean viral titers for 3 animals for each time point. Error bars indicate standard errors of the mean. *P<0.05, **P<0.01 and ***P<0.001 (unpaired t test). Mock, mice without infection. Data are representative of three independent experiments with similar results (mean + s.d.).