| Literature DB >> 8909235 |
V G Sasseville1, M M Smith, C R Mackay, D R Pauley, K G Mansfield, D J Ringler, A A Lackner.
Abstract
The pathogenesis of neurological dysfunction associated with human immunodeficiency (HIV)-1 infection is uncertain. However, the presence of macrophage infiltrates in the central nervous system is a key feature of HIV encephalitis and is correlated with HIV-associated dementia. Moreover, it has been demonstrated that HIV-infected monocyte/macrophages can produce toxic substances that may play a critical role in the development of HIV-associated dementia. However, the exact mechanisms responsible for HIV infection and leukocyte recruitment to the central nervous system remain speculative. Similar to HIV-infected patients, simian immunodeficiency virus (SIV)-infected macaque monkeys develop immunosuppression and acquired immune deficiency syndrome (AIDS)-related inflammatory disorders, including AIDS encephalitis. In this study, we demonstrate that encephalitic brain from SIV-infected animals has elevated immunohistochemical expression of the C-C chemokines, macrophage inflammatory protein-1 alpha and -beta, RANTES, and monocyte chemotactic protein-3, and the C-X-C chemokine interferon-inducible protein-10. These findings suggest that one or all of of these chemokines could be involved in leukocyte recruitment to the brain in SIV-infected macaque monkeys.Entities:
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Year: 1996 PMID: 8909235 PMCID: PMC1865261
Source DB: PubMed Journal: Am J Pathol ISSN: 0002-9440 Impact factor: 4.307