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- Howard E Gendelman
- Department of Medicine , Manhasset, New York
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- Stuart A Lipton
- Department of Laboratory of Cellular and Molecular Neuroscience, Childrens Hospital and Harvard Medical School , Boston, Massachusetts
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- Marc Tardieu
- Department of ANRS Universite Paris XI, Hopital Bicetre , Bicetre , France
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- Michael I Bukrinsky
- Department of The Picower Institute , Manhasset, New York
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- Hans S L M Nottet
- Department of Pathology and Microbiology, and the Manhasset , New York
説明
<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>
収録刊行物
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- Journal of Leukocyte Biology
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Journal of Leukocyte Biology 56 (3), 389-398, 1994-09-01
Oxford University Press (OUP)