Abstract
Long before the discovery of the human immunodeficiency viruses, HTV-1 and HIV-2, studies with visna virus and other lentiviruses of ruminants established that neuroinvasiveness and neuroviru-lence are a characteristic of lentiviral infections (Nathanson, 1998). Soon after the first descriptions of the acquired immunodeficiency syndrome (AIDS), landmark studies by Price and others (Price et al, 1988) established the importance of neurological symptomatology in a significant proportion of HIV infected individuals. The neurological deterioration attributed to HIV infection itself (as opposed to the problems associated with opportunistic infection) has been described extensively in many reviews, but can be briefly summarized as a subcortical dementia, differing from cortical dementias by the tendency for memory impairment to occur after other cognitive symptoms like inattention, indifference, and psychomotor slowing (reviewed in Atwood et al, 1993; McArthur et al, 1994), and by prominent motor abnormalities like incoordination. This symptom complex has been termed the AIDS Dementia Complex (ADC), or HIV Dementia (HIVD). Its neuropathological correlate, HIV encephalitis (HIVE), consists of a constellation of findings that includes myelin pallor, astrocytosis, and most specifically for HIV infection, the formation of multinucleated giant cells (MGC's) that are thought to be the result of syncytia formation between infected macrophages and microglia (Sharer, 1992; Wiley and Achim, 1994). Syncytia formation is a common tissue culture signature for HIV infection and is the result of the interaction between the viral envelope proteins (gpl20 and gp4l) and the cellular receptors for the virus.