Figure 6From: T-cell reconstitution during murine acquired immunodeficiency syndrome (MAIDS) produces neuroinflammation and mortality in animals harboring opportunistic viral brain infection Lethal disease was associated with exacerbated neuroinflammation. (A) Schematic representation of the experimental design. In brief, C57BL/6 mice with murine acquired immunodeficiency syndrome (MAIDS) (8 wks post-LP-BM5 infection) were super-infected with herpes simplex virus (HSV)-1 through i.n. inoculation. T-cell reconstitution was induced 7 d post-HSV infection through adoptive transfer of 5 x 106 CD3+ cells obtained from primed donor animals via tail vein injection. Brain tissues were harvested from the LP-BM5 + HSV and LP-BM5 + HSV + CD3AT groups 7 d post-adoptive transfer (p.t.). (B) Brain leukocytes were collected and labeled with PE-Cy5-conjugated antibodies specific for CD45, AF700-labeled anti-CD11b, and allophycocyanin-labeled major histocompatability complex (MHC) class II. Brain-resident CD45intCD11b+ microglial cells were analyzed for the activation marker MHC class II. Histograms showing pooled data from three independent experiments are shown. Data are presented as mean ± standard error percentage of CD45intCD11b+ cells displaying MHC class II expression. (C) mRNA expression for the indicated proinflammatory mediators was assessed using real-time quantitative reverse-transcribed PCR on total RNA extracted from brain stem homogenates at 7 d p.t. Levels of mRNA were normalized to hypoxanthine guanine phosphoribosyl transferase-1 and are presented as mean ± SD normalized to LP-BM5 control from pooled data obtained using five animals per group from three independent experiments. * P <0.05 versus LP-BM5 + HSV-infected mice.Back to article page