IMR Press / FBL / Volume 13 / Issue 10 / DOI: 10.2741/2979

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
Roles of MCP-1 in development of HIV-dementia
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1 Molecular and Integrative Physiology Department, University of Kansas Medical Center, Kansas City, KS
2 Microbiology, Molecular Genetics and Immunology Department, University of Kansas Medical Center, Kansas City, KS

*Author to whom correspondence should be addressed.

Academic Editor: Francesca Peruzzi

Front. Biosci. (Landmark Ed) 2008, 13(10), 3913–3918;
Published: 1 May 2008
(This article belongs to the Special Issue Molecular basis of neuronal dysfunction in AIDS)

The encephalopathy caused by HIV, known clinically as HIV-associated dementia (HAD) and pathologically as HIV encephalitis (HIVE), results from intense infiltration of mononuclear cells, productive replication of the virus in monocyte-derived macrophages/microglia, abortive replication in astrocytes and activation of macrophages/microglia and astrocytes leading to neuronal degeneration in the brains of infected persons. Recent findings have suggested that development of HAD is based more on the activation process than on direct evidence of virus replication in the brain. Since HAD is based on the encephalitic process, major studies have been directed to the mechanisms regulating the inflammatory process. Monocyte chemoattractant protein 1, MCP-1, is a chemokine that is implicated in this process and also in the development of activation in the brain. In this review, we have attempted to identify mechanisms that induce expression of MCP-1 in the brain and the role that it plays in recruitment of mononuclear cells from blood to brain and in the activation processes of inflammatory and neural cells that lead to development of degenerative changes in the neuronal population.

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