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. 2019 Jan 1;15(2):481–492. doi: 10.7150/ijbs.25862

Figure 6.

Figure 6

CD163 modification significantly inhibits PRRSV replication in pigs. (A) Rectal temperature curves (left), clinical sign score (middle) and body weight curves (right) of pigs from two challenged groups after PRRSV JXA1 infection. WT group, n=6. CD163Mut/Mut group, n=4. Scoring was based on the appearance of respiratory distress, inappetence, lethargy and fever (see 'Materials and methods'). Because of the considerable difference between #8 #9 pigs and #10 #12 pigs in the CD163Mut/Mut group, data for these pigs were analyzed separately. (B) Viral load in pigs of the two groups. (left) Analysis of viral load in the serum of pigs from the two groups at indicated time points. (right) Relative expression of viral RNA in lungs of the infected pigs. Samples were collected from the lungs of dying challenged pigs. Data in panels A-B are presented as the mean±SD. * P<0.05, ** P<0.01, *** P<0.001. (C) Survival curves for pigs from the two challenged groups after infection with PRRSV JXA1. CD163Mut/Mutpigs survived significantly longer than WT pigs. (D) Macroscopic lesion, histopathology and immunohistochemical staining of lungs and tonsils from infected pigs. (top) Diseased lungs and tonsils of pigs in different groups showed different damage extent. (middle) Representative photomicrographs of HE-stained tissues from WT and CD163Mut/Mut pigs. (bottom) Representative photomicrographs of immunohistochemically stained tissues from WT and CD163Mut/Mut pigs. PRRSV (red) was visualized via a monoclonal antibody recognizing the viral nucleocapsid protein.