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Cellular aspects of HIV‐1 infection of macrophages leading to neuronal dysfunction in in vitro models for HIV‐1 encephalitis
Author(s) -
Nottet Hans S. L. M.,
Bär Dop R.,
Hassel Hans,
Verhoef Jan,
Boven Leonie A.
Publication year - 1997
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.62.1.107
Subject(s) - biology , human immunodeficiency virus (hiv) , in vitro , encephalitis , immunology , virology , neuroscience , virus , genetics
Abstract HIV‐1 is a hematogenously spread virus that most likely gains entry into the brain within blood‐derived macrophages. Indeed, productive viral replication selectively occurs within perivascular and parenchymal blood‐derived macrophages and microglia and HIV‐infected macrophages have increased potential to bind and transmigrate through the blood‐brain barrier. Once inside the brain, HIV‐infected macrophages secrete a variety of proinflammatory mediators that display neuromodulatory and neurotoxic activities in several in vitro models for HIV‐1 encephalitis. The final outcome regarding neuronal function and cell loss is regulated through intercellular interactions between these virus‐infected cells and astrocytes. In this regard, both HIV‐induced intracellular events in macrophages and interactions between HIV‐infected macrophages and brain cells are reviewed as factors that might lead to neuronal injury in in vitro model systems for HIV‐1 encephalitis. J. Leukoc. Biol . 62: 107–116; 1997.