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Department of Neuropharmacology, The Scripps Research Institute, La Jolla, CA 92037
One of the consequences of HIV infection is damage to the CNS. To
characterize the virologic, immunologic, and functional factors
involved in HIV-induced CNS disease, we analyzed the viral loads and T
cell infiltrates in the brains of SIV-infected rhesus monkeys whose CNS
function (sensory evoked potential) was impaired. Following infection,
CNS evoked potentials were abnormal, indicating early CNS disease. Upon
autopsy at 11 wk post-SIV inoculation, the brains of infected animals
contained over 5-fold more CD8+ T cells than did uninfected
controls. In both infected and uninfected groups, these
CD8+ T cells presented distinct levels of activation
markers (CD11a and CD95) at different sites: brain > CSF >
spleen = blood > lymph nodes. The CD8+ cells
obtained from the brains of infected monkeys expressed mRNA for
cytolytic and proinflammatory molecules, such as granzymes A and B,
perforin, and IFN-
. Therefore, the neurological dysfunctions
correlated with increased numbers of CD8+ T cells of an
activated phenotype in the brain, suggesting that virus-host
interactions contributed to the related CNS functional
defects.
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