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Magnetic resonance spectroscopy reveals a role of activated monocytes contributing to neuronal injury in simian immunodeficiency virus neuroAIDS
Aug 19, 2005, 13:47, Reviewed by: Dr.
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This data underscores the role of the continuous traffic of activated and infected monocytes to the CNS that is required for CNS disease and neuronal injury in this model, and shows the role of plasma virus, monocytes, and CD8 T lymphocytes outside of the brain in controlling CNS disease.
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By Journal of Clinical Investigation,
About 30% of patients with HIV also develop neurological symptoms, but the mechanisms by which the immune system contributes to central nervous system (CNS) disease were unclear.
In a study appearing online on August 18 in advance of print publication of the September 1 issue of the Journal of Clinical Investigation, Kenneth Williams and colleagues from Beth Israel Deaconess Medical Center use a model of neuroAIDS in rhesus monkeys infected with Simian Immunodeficiency Virus (SIV).
The researchers document changes in blood monocyte activation and SIV infection that occur with neuronal injury. They also use combination anti-retroviral therapy on the monkeys during primary infection, and show little effect on plasma viral load, but inhibition of subsequent activation and infection of blood monocytes. The inhibition of blood monocyte activation and infection with retroviral therapy rapidly reduces CNS neuronal injury. Animals on retroviral therapy show no accumulation of macrophages in the CNS or detectable virus, in contrast to non-treated animals.
This data underscores the role of the continuous traffic of activated and infected monocytes to the CNS that is required for CNS disease and neuronal injury in this model, and shows the role of plasma virus, monocytes, and CD8 T lymphocytes outside of the brain in controlling CNS disease. 
- September 1 issue of the Journal of Clinical Investigation
Journal of Clinical Investigation
AUTHOR CONTACT:
Kenneth Williams
Beth Isreal Deaconess Medical Center, Boston, MA USA
Phone: 617 667 2064; Fax: 617 667 8210; E-mail: [email protected]
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