Document 0288 DOCN M9590288 TI HIV neuropathology: consequences of direct infection. DT 9509 AU Gonzales M; Neuropathology Research Laboratory, Royal Melbourne Hospital,; Parkville, VIC. SO Annu Conf Australas Soc HIV Med. 1994 Nov 3-6;6:222 (unnumbered abstract). Unique Identifier : AIDSLINE ASHM6/95291811 AB The appearance of HIV-specific antibodies in CSF soon after seroconversion and the subsequent development of a range of neuropathological changes reflect HIV neurotropism. Lymphoma and a range of opportunistic infections are components of the spectrum of HIV-related CNS pathology but a slowly developing encephalopathy involving white and deep grey matter appears to be a consequence of direct CNS infection. This encephalopathy contributes to a clinical syndrome of motor and cognitive deficits for which HIV-1 associated cognitive/motor complex has been suggested. The essential pathological features of this complex include microglial nodules containing multinucleated giant cells (MNGC's) in white matter, vacuolation of myelin and astrocytic proliferation. There is also a variable degree of cortical neuronal loss and reduction in synaptic density. Intrinsic microglial cells and the MNGC's, formed from bone marrow derived monocyte/macrophages appear to be the only cells that are productively infected. However there are some data to suggest restrictive infection of astrocytes, particularly in young children with encepahalopathy. The pathology of the HIV-associated cognitive/motor complex appears to be an indirect consequence of infection of MNGC's and microglia, mediated through gp120, cytokines, in particular TNF-a and arachidonic acid metabolites. Some of these activate neuronal NMDA receptors. Neuronal loss may be related to nitric oxide toxicity. A similar mechanism resulting in degeneration of dorsal root ganglia neurones may contribute to the distal predominantly sensory neuropathy which is commonly seen in patients with AIDS. DE Acquired Immunodeficiency Syndrome/PATHOLOGY Adult Astrocytes/PATHOLOGY AIDS Dementia Complex/*PATHOLOGY Child Ganglia, Spinal/PATHOLOGY Human Motor Neuron Disease/*PATHOLOGY Nerve Degeneration/PHYSIOLOGY Syndrome MEETING ABSTRACT SOURCE: National Library of Medicine. NOTICE: This material may be protected by Copyright Law (Title 17, U.S.Code).