Fig. 4
IFNAR signaling of neuroectodermal cells restricts viral load in the cerebrum at 4 days after TMEV-BeAn infection. A Viral antigen in the hippocampus of TMEV-infected IFNAR−/−, NesCre±IFNARfl/fl, GFAPCre±IFNARfl/fl, Syn1Cre±IFNARfl/fl and Cre−/−IFNARfl/fl mice as well as tamoxifen (Tam)-treated Sall1CreER± mice and Sall1CreER−/− control mice. Immunohistochemistry using the avidin–biotin-peroxidase complex method with the chromogen 3′3-diaminobenzidine and Mayer’s hematoxylin counterstaining. B Semiquantitative analysis of immunohistochemically stained coronal brain sections cut at the level of the hippocampus (1 complete section per mouse evaluated) did not detect significant differences in the amount of viral antigen between the mouse groups (IFNAR−/−: n = 6; NesCre±IFNARfl/fl: n = 10; GFAPCre±IFNARfl/fl: n = 9; Syn1Cre±IFNARfl/fl: n = 10; Cre−/−IFNARfl/fl: n = 7; Sall1CreER±: n = 6; Sall1CreER−/−: n = 9). C Quantification of TMEV RNA in the cerebrum using RT-qPCR revealed a higher viral load in IFNAR−/− (n = 6), NesCre±IFNARfl/fl (n = 8) and GFAPCre±IFNARfl/fl mice (n = 8) but not Syn1Cre±IFNARfl/fl mice (n = 6) compared to Cre−/−IFNARfl/fl mice (n = 5). Similar numbers of viral transcripts in tamoxifen (Tam)-treated Sall1CreER± mice (n = 6) and Sall1CreER−/− control mice (n = 8). Mann–Whitney tests using the Bonferroni correction for multiple comparisons: * p < 0.05; ** p < 0.01. Shown are all data points with means. Each data point represents the semiquantitative score (B) or the TMEV RNA copy number (C) of one mouse