The neuropathogenesis of HIV-1 infection

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  • Howard E Gendelman
    Department of Medicine , Manhasset, New York
  • Stuart A Lipton
    Department of Laboratory of Cellular and Molecular Neuroscience, Childrens Hospital and Harvard Medical School , Boston, Massachusetts
  • Marc Tardieu
    Department of ANRS Universite Paris XI, Hopital Bicetre , Bicetre , France
  • Michael I Bukrinsky
    Department of The Picower Institute , Manhasset, New York
  • Hans S L M Nottet
    Department of Pathology and Microbiology, and the Manhasset , New York

Description

<jats:title>Abstract</jats:title> <jats:p>HIV infection in brain revolves around productive viral replication in cells of mononuclear phagocyte lineage, including brain macrophages, microglia, and multinucleated giant cells [1–4]. Together, they are the instigators for cellular and viral neurotoxic activities [5–10]. Several published reports show that viral and/or cellular products produced from HIV-1-infected macrophages injure neurons and induce glial proliferation during advancing central nervous system (CNS) infection [11–18]. These findings are supported by the apparent discrepancy between the distribution and numbers of virus-infected cells and concomitant brain tissue pathology [5, 19]. Whether these soluble factors are indirectly responsible for neuronal damage remains undefined. The identification and regulation of neurotoxins produced from HIV-infected macrophages are central to uncovering how HIV mediates CNS disease. The authors who contributed to this work represent laboratories with overlapping areas of expertise. Broad-based complementary hypotheses regarding HIV neuropathogenesis are now provided. J. Leukoc. Biol. 56: 389–398; 1994.</jats:p>

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