       Document 0035
 DOCN  M9630035
 TI    Role of HIV in the pathogenesis of distal symmetrical peripheral
       neuropathy.
 DT    9603
 AU    Rizzuto N; Cavallaro T; Monaco S; Morbin M; Bonetti B; Ferrari S;
       Galiazzo-Rizzuto S; Zanette G; Bertolasi L; Department of Neurological
       and Visual Sciences, University of; Verona, Italy.
 SO    Acta Neuropathol (Berl). 1995;90(3):244-50. Unique Identifier : AIDSLINE
       MED/96049767
 AB    We report the results of a clinical, electrophysiological and
       pathological study conducted in 18 AIDS patients presenting a distal
       symmetrical predominantly sensory polyneuropathy (DSPN) characterized by
       painful dysesthesias as main complaint. Onset of the neuropathy was at
       CDC (Center for Disease Control) stage II in 2 patients, at CDC stage
       III in 5 patients and at CDC stage IV in the remainder.
       Electrophysiological investigation confirmed the presence of an axonal
       alteration in the sensory nerves, but also revealed motor involvement in
       all cases. The neuropathological features of sensory nerves were fiber
       loss and axonal degeneration with macrophagic activation. The expression
       of monocyte-macrophage markers and of major histocompatibility complex
       class II antigens appeared up-regulated in endoneurial ramified cells,
       while expression of CR3, a complement receptor involved in the process
       of phagocytosis, was down-regulated. In six nerve biopsy samples and in
       two out of five DSPN dorsal root ganglia we found HIV-related mRNA and
       protein located in scattered cells of the endoneurium which we presume
       to be macrophages. These data suggest that: (a) DSPN may occur early in
       the course of the disease and is not limited to later stages; (b) DSPN
       is not a ganglionitis but is actually a sensory-motor neuropathy; (c)
       the virus enters the peripheral nervous system and induces changes in
       the immunocompetent cell population with activation of macrophages.
       Storage of the virus inside macrophages may act both as a reservoir for
       the virus and as a putative cause of nerve damage, probably through
       release of cytotoxins and/or interaction with trophic factors.
 DE    Acquired Immunodeficiency Syndrome/*COMPLICATIONS  Adult  Autopsy
       Biopsy  Electrophysiology  Female  Ganglia, Spinal/*PATHOLOGY  Human
       HIV  Immunohistochemistry  In Situ Hybridization  Male  Middle Age
       Peripheral Nervous System/*PATHOLOGY  Support, Non-U.S. Gov't  JOURNAL
       ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

