Abstract

Rhesus monkeys infected with simian immunodeficiency virus (SIV), a lentivirus closely related to human immunodeficiency virus (HIV), develop AIDS and encephalopathy with a frequency similar to that of HIV-infected humans. The pathogenic relationships among systemic virus infection, central nervous system (CNS) inflammation and immune activation, viral infection of the CNS, and clinical encephalopathy are still very poorly understood in HIV disease. Most puzzling is the apparent lack of correlation between extent of virus infection and degree of encephalopathy in human AIDS. This has focused attention on indirect mechanisms of viral insult to the brain. These include generation of neurotoxins and inflammatory mediators in the CNS, and activation or dysregulation of microglia, glia, and neurons. Cellular and neurochemical processes triggered initially by virus infection and leading to encephalopathy can be systematically studied in the SIV-infected rhesus monkey. These same processes, perhaps triggered by other viruses, or by inflammatory events occuring during critical periods of development, may also be involved in other types of human encephalopathy. © 1997 Wiley-Liss, Inc. This article is a US Government work and, as such, is in the public domain in the United States of America.

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