Document 0286
 DOCN  M9590286
 TI    Cytokine aspects of the neuropathogenesis of HIV infection.
 DT    9509
 AU    Wesselingh SL; Glass J; McArthur J; Griffin J; Griffin DE; Department of
       Microbiology and Infectious Diseases, Flinders; University, Bedford
       Park, South Australia.
 SO    Annu Conf Australas Soc HIV Med. 1994 Nov 3-6;6:224 (unnumbered
       abstract). Unique Identifier : AIDSLINE ASHM6/95291813
 AB    AIDS is associated with three major neurological syndromes:
       HIV-Associated Dementia, Vacuolar Myelopathy and Predominantly Sensory
       Neuropathy. The central role of cytokines in the pathogenesis of these
       HIV-associated neurological diseases is now beyond doubt. Initial
       studies of cerebrospinal fluid indicated clearly that there was
       increased levels of inflammatory markers in the CSF of patients with
       neurological disease. Subsequent studies utilising immunohistochemical
       techniques then demonstrated clear evidence of increased cytokine
       expression in the brains, spinal cord and peripheral nerves of HIV
       infected patients with neurological disease. Consistent with these
       findings, morphological studies have demonstrated a marked increase in
       the number of activated macrophages/microglia in neurological tissue of
       patients with HIV-associated neurological disease suggesting a loss of
       macrophage regulation. Utilising molecular techniques a consistent
       profile of increased TNF alpha and decreased IL4 was found in all three
       syndromes compared to AIDS patients without neurological disease. HIV
       transcripts were increased in the HIV-associated Dementia brains
       compared to nondemented controls but were detected less often in spinal
       cord and not at all in peripheral nerve. Data from in situ RT/PCR
       suggests that a large number of macrophages/microglia are expressing TNF
       but only small number are infected with HIV. The finding of elevated TNF
       alpha expression associated with increased macrophage activation and
       decreased IL4 suggests that the loss of a subset of T cells expressing
       macrophage regulatory lymphokines such as IL4 and IL10 may explain the
       observed macrophage activation seen in the neurological diseases
       associated with AIDS and play a role in the development of
       neuropathology and/or neuronal dysfunction.
 DE    AIDS Dementia Complex/*IMMUNOLOGY  Cytokines/*PHYSIOLOGY  Human
       Interleukin-4/PHYSIOLOGY  Macrophage Activation/*IMMUNOLOGY  Nervous
       System Diseases/*IMMUNOLOGY  Peripheral Nerves/IMMUNOLOGY  Spinal
       Cord/IMMUNOLOGY  T-Lymphocytes/IMMUNOLOGY  Tumor Necrosis
       Factor/PHYSIOLOGY  MEETING ABSTRACT

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