NDLI: New Insights into the Neuroimmunity of SIV Infection by Magnetic Resonance Spectroscopy

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Neuroimmunity and the Blood–Brain Barrier: Molecular Regulation of Leukocyte Transmigration and Viral Entry into the Nervous System with a Focus on NeuroAIDS

Neurobiology of Multiple Insults: HIV-1-Associated Brain Disorders in Those Who Use Illicit Drugs

Journal of Neuroimmune Pharmacology : Volume 1, Issue 1, March 2006

New Insights into the Neuroimmunity of SIV Infection by Magnetic Resonance Spectroscopy

Content Provider	Springer Nature Link
Author	González, R. Gilberto Greco, Jane B. He, Julian Lentz, Margaret R. O'Neil, Shawn Pilkenton, Sarah J. Ratai, Eva M. Westmoreland, Susan
Copyright Year	2006
Abstract	$^{1}$H magnetic resonance spectroscopy (MRS) was employed to noninvasively monitor neuronal injury in eight rhesus macaques infected with simian immunodeficiency virus (SIV), whose immune system was compromised by CD8 T lymphocyte depletion and treated with highly active antiretroviral therapy (HAART). SIV infection and CD8 depletion resulted in a rapid decline in cerebral N-acetylaspartate (NAA) levels, a sensitive marker of neuronal health. Within 3 months of SIV infection and CD8 depletion, four animals developed AIDS and severe SIV encephalitis. The other four macaques underwent daily doses of HAART beginning 4 weeks after infection/CD8 depletion. HAART involved drugs that do not penetrate the central nervous system (CNS) including 9-[2(R)-(phosphonomethoxy)propyl]adenine and a racemic mixture of d-l-enantiomers of 2′,3′-dideoxy-5-fluoro-3′thiacytidine. HAART resulted in reversal of NAA/Cr decline after 4 weeks of therapy, and no virus or encephalitis was found in brain samples analyzed. These results indicate that the CNS injury in AIDS is entirely dependent on events involving the peripheral immune system mediated by trafficking of SIV-infected monocytes into the brain. The rapid decline in NAA/Cr with SIV infection/CD8 depletion and its rapid recovery with HAART suggest that: (1) infected monocyte turnover in the CNS is rapid, occurring in days to weeks; (2) there are endogenous mechanisms that reverse neuronal injury; and (3) a threshold level of infected monocytes/macrophages in the CNS is required to overcome the neuronal recovery processes. These observations explain the clinical success of antiretroviral therapy in reducing the incidence of HIV-associated dementia and minor cognitive/motor disorder and suggest novel targets for drug development.
Starting Page	152
Ending Page	159
Page Count	8
File Format	PDF
ISSN	15571890
Journal	Journal of Neuroimmune Pharmacology
Volume Number	1
Issue Number	2
e-ISSN	15571904
Language	English
Publisher	Springer US
Publisher Date	2006-03-21
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	MR spectroscopy neuroAIDS Simian immunodeficiency virus (SIV) CD8 T lymphocyte Highly active antiretroviral therapy (HAART) N-acetylaspartate (NAA) AIDS SIV encephalitis Monocytes CNS Macrophages HIV-associated dementia Cell Biology Virology Pharmacology/Toxicology Immunology Neurosciences
Content Type	Text
Resource Type	Article
Subject	Neuroscience Immunology and Allergy Pharmacology Immunology

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