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Analysis of Simian Immunodeficiency Virus-specific CD8+ T-cells in Rhesus Macaques by Peptide-MHC-I Tetramer Staining
Published on: December 23, 2016
Active simian immunodeficiency virus (strain smmPGm) infection in macaque central nervous system correlates with
Marilyn S Smith1, Yafen Niu, Shilpa Buch
1Marion Merrell Dow Laboratory of Viral Pathogenesis, University of Kansas Medical Center, Kansas City, KS 66160, USA. msmith6@kumc.edu
Abstract:
Simian immunodeficiency virus strain smmPGm can induce neuropathology in macaques and is a model for the development of human HIV-related brain injury. For quantitative studies of proviral presence and expression in the central nervous system (CNS), we inoculated 8 macaques intravenously with the virus. Three animals were necropsied 2 to 4 weeks after development of infection, and we obtained lymphoid tissue biopsies from 5 animals before 5 weeks after infection. Peak plasma viral loads averaged 10 viral RNA Eq/mL at week 2, whereas cerebrospinal fluid viral loads peaked at 10 viral RNA Eq/mL. The proviral DNA loads and viral gag mRNA expression in tissues were quantified by real-time polymerase chain reaction. Two animals developed neurologic disease characterized by meningoencephalitis and meningitis. Proviral DNA levels in CNS tissues of these animals at necropsy revealed 10 and 10 copies/microg of DNA, respectively, whereas viral RNA expression in the CNS reached 100 to 1000 times higher levels than those seen in early necropsies. In sharp contrast, in 2 animals necropsied at later times without CNS disease, virus mRNA expression was not detected in any CNS tissue. Our results are consistent with the hypothesis that active virus expression in the CNS is strongly correlated with neurologic disease and that the event occurs at variable periods after infection.
Insights
Simian immunodeficiency virus (SIV) infection in macaques can cause brain injury, similar to human HIV. Active SIV replication in the central nervous system (CNS) correlates with neurological disease development.
Area of Science:
- Neuroscience
- Virology
- Immunology
Background:
- Simian immunodeficiency virus (SIV) infection in macaques serves as a crucial model for understanding human immunodeficiency virus (HIV)-related central nervous system (CNS) neuropathology.
- Neuropathology in SIV-infected macaques offers insights into HIV-associated brain injury mechanisms.
Purpose of the Study:
- To quantitatively assess proviral DNA and viral RNA expression within the CNS of SIV-infected macaques.
- To investigate the correlation between viral presence/expression in the CNS and the development of neurological disease.
Main Methods:
- Intravenous inoculation of macaques with SIV strain smmPGm.
- Quantitative analysis of proviral DNA and gag mRNA in lymphoid and CNS tissues using real-time polymerase chain reaction (PCR).
- Monitoring of plasma and cerebrospinal fluid viral loads.
Main Results:
- Two out of eight macaques developed meningoencephalitis and meningitis.
- Animals with neurological disease exhibited high proviral DNA loads (10^4-10^5 copies/microg) and significantly elevated viral RNA expression (100-1000x higher) in CNS tissues.
- In contrast, macaques without CNS disease showed no detectable viral RNA expression in the CNS.
Conclusions:
- Active viral replication within the CNS is strongly associated with the development of SIV-induced neuropathology.
- The onset of active CNS viral expression and subsequent neurological disease can occur at variable times post-infection.
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