Loss of central nervous system viral control in CD4-depleted B7-H1
mice. Infected wild-type (WT) and B7-H1−/− mice were treated with α-CD4 or control α-βgalactosidase (α-βgal) monoclonal antibody (mAb) at 4 and 6 days post-infection (p.i). (A) Virus titers in the brain determined by plaque assay expressed as mean ± SEM. Dashed line represents limit of detection. Significant differences between CD4-depleted and CD4-undepleted mice were determined by the unpaired t-test. * P<0.05 and *** P<0.001, respectively. Significant differences comparing CD4 depleted WT and B7-H1−/− mice were determined by the unpaired t-test. #
P<0.05 and ###
P<0.001, respectively. (B) Virus-infected cells detected in spinal-cord white-matter tracks using α-nucleocapsid mAb (J.3.3; brown) with hematoxylin counterstain at 10 days p.i. (C) Double immunohistochemical staining with rabbit α-glutathione S-transferase (α-GST) antibody labeling the oligodendrocytes (brown; DAB chromogen) and α-nucleocapsid J.3.3 mAb (blue/grey SG chromogen). Arrows point to virus-infected oligodendroglial cells (double-labeled), adjacent to non-infected oligodendroglial cells (labeled with DAB only). Magnification bar = 10 μm. (D) Frequencies of virus-specific interferon (IFN)-γ secreting CD8 T cells per 106 CD8 T cells in CLNs at day 5 and 7 p.i. detected by flow cytometry after S510 peptide stimulation. Data are representative of two independent experiments with four mice per time point per experiment.