Fig 2: Strong TSPO immunoreactivity in a subset of tyrosine hydroxylase+ neurons in the striatum. a–f Representative samples of double-label immunostained 5 µm brain sections for TSPO (red) and Iba-1 (brown). a Buffer OPN+, b HIV OPN+, c HIV OPN+, d Buffer OPN-, e HIV OPN-, f Buffer OPN-. g hematoxylin/eosin stained section, and serial adjacent sections stained with h TSPO and i tyrosine hydroxylase. The black ovals demarcate the region of interest in each section

Fig 3: Iba-1 but not TSPO immunoreactivity is increased in the brains of mice suppressed for osteopontin. Quantitative analyses of TSPO or Iba-1 antibody reactivity, Buffer-OPN+ n = 3, Buffer-OPN- n = 4, HIV-OPN+, n = 3; HIV-OPN-, n = 4; nested one-way ANOVA with Tukey’s for multiple comparisons. The mean and standard deviation (graphs), with significant intragroup differences (P < .0001, chi-square, df 17.68, 1), but no significant intergroup differences (ns) is shown

Fig 4: Robust TSPO immunoreactivity in a subset of neurons in the cerebellum. a–e Representative samples of double-label immunostained 5 µm brain sections for TSPO (red) and Iba-1 (brown) and their corresponding hematoxylin/eosin near adjacent section are shown a Buffer-OPN+, b HIV-OPN+, c HIV-OPN+, d Buffer-OPN-, and e HIV-OPN-. An ordered array of Purkinje neurons was not visible in HIV-infected mice lacking osteopontin (e, HIV-OPN-) compared to d HIV-OPN+. f Enlarged area from d, e is shown with the white matter, Purkinje, granular, and molecular layers of the cerebellum indicated by the arrows