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. 2024 Mar 29;39(3):434–446. doi: 10.1016/j.virs.2024.03.010

Fig. 3.

Fig. 3

Characterization of VSV-EBOV/GP infection in 3-week-old Syrian hamsters. A Three-week-old Syrian hamsters were intraperitoneally infected with VSV-EBOV/GP (107 TCID50). B Animals were monitored for weight changes, temperature changes, and survival. C, D Blood biochemistry and blood cell count were analyzed at 1.5 days post-infection. E Viral loads including hearts, livers, spleens, lungs, kidneys, stomachs, intestines, and brains were determined at 1.5 days post-infection. Data presented as mean ​± ​SEM. Statistical analyses were performed using One-way ANOVA. ∗, P ​< ​0.05; ∗∗, P ​< ​0.01; ∗∗∗, P ​< ​0.001; ∗∗∗∗, P ​< ​0.0001. F Severe uveitis was observed in the eyes of VSV-EBOV/GP infected animals. G, H Histopathological and immunohistochemistry assays of the liver, spleen, lung and kidney at 1.5 days post-infection. Scale bar ​= ​100 ​μm. Hepatic lesions including hepatocellular necrosis, nuclear fragmentation (black arrows), lymphocytic infiltration (blue arrows), granulocytic infiltration (green arrows), and hepatocellular steatosis (yellow arrows) were observed. Splenic lesions including lymphocytic necrosis with nuclear fragmentation (black arrows), cellular necrosis with nuclear fragmentation (blue arrows), neutrophilic infiltrate (green arrows), and bruising (yellow arrows) were observed. Lung tissue showed diffuse mild thickening of the alveolar wall, narrowing or loss of the alveolar lumen with inflammatory cell infiltration (black arrows); bronchial epithelial cells were detached (blue arrows). Kidney lesions were seen as hydropic degeneration of renal tubular epithelial cells (black arrows) and dilatation of renal tubular interstitial vessels seen as stasis (blue arrows).