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Updated: Jul 16, 2026
Analysis of Simian Immunodeficiency Virus-specific CD8+ T-cells in Rhesus Macaques by Peptide-MHC-I Tetramer Staining
Published on: December 23, 2016
Highly activated CD8(+) T cells in the brain correlate with early central nervous system dysfunction in simian
M C Marcondes1, E M Burudi, S Huitron-Resendiz
1Department of Neuropharmacology, The Scripps Research Institute, La Jolla, CA 92037, USA.
Insights
HIV infection damages the central nervous system (CNS). Increased activated CD8(+) T cells in the brain correlate with neurological dysfunction in SIV-infected monkeys, suggesting virus-host interactions contribute to CNS disease.
Area of Science:
- Neuroscience
- Immunology
- Virology
Background:
- Human Immunodeficiency Virus (HIV) infection can lead to central nervous system (CNS) damage.
- Understanding the mechanisms of HIV-induced CNS disease is crucial for developing effective treatments.
Purpose of the Study:
- To characterize virologic, immunologic, and functional factors in HIV-induced CNS disease.
- To investigate the role of T cell infiltrates and viral loads in the brains of SIV-infected rhesus monkeys with impaired CNS function.
Main Methods:
- Analysis of viral loads and T cell infiltrates in the brains of SIV-infected rhesus monkeys.
- Measurement of CNS function using sensory evoked potentials.
- Assessment of CD8(+) T cell activation markers (CD11a, CD95) and gene expression (cytolytic and proinflammatory molecules).
Main Results:
- SIV-infected monkeys exhibited abnormal CNS evoked potentials, indicating early CNS disease.
- Brains of infected animals showed a 5-fold increase in CD8(+) T cells compared to controls.
- Activated CD8(+) T cells in infected brains expressed mRNA for cytolytic and proinflammatory molecules like granzymes, perforin, and IFN-gamma.
Conclusions:
- Neurological dysfunctions in SIV-infected monkeys correlated with increased numbers of activated CD8(+) T cells in the brain.
- These findings suggest that virus-host interactions contribute to CNS functional defects in HIV infection.
Abstract:
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-gamma. 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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