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.