Microarray analysis of cytokine and chemokine genes in the brains of macaques with SHIV-encephalitis

:  Human immunodeficiency virus (HIV)‐encephalitis results from a cascade of viral–host interactions that lead to cytokine and chemokine imbalance, which then leads to neuropathologic manifestations of the disease. These include macrophage/microglia activation, astrocytosis and neuronal dysfunction...

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Published in:Journal of medical primatology 2003-08, Vol.32 (4-5), p.229-239
Main Authors: Sui, Yongjun, Potula, Raghava, Pinson, David, Adany, Istvan, Li, Zhuang, Day, Jason, Buch, Eisha, Segebrecht, Jane, Villinger, Francois, Liu, Zhenqian, Huang, Mingzhao, Narayan, Opendra, Buch, Shilpa
Format: Article
Language:English
Subjects:
Animals
Brain - immunology
Brain - virology
chemokines
cytokines
DNA Primers
Encephalitis, Viral - genetics
Gene Expression Regulation
HIV Infections
Immunohistochemistry
Macaca mulatta
neuropathology
Oligonucleotide Array Sequence Analysis
Receptors, Chemokine - genetics
Reverse Transcriptase Polymerase Chain Reaction
Simian Acquired Immunodeficiency Syndrome
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Summary::  Human immunodeficiency virus (HIV)‐encephalitis results from a cascade of viral–host interactions that lead to cytokine and chemokine imbalance, which then leads to neuropathologic manifestations of the disease. These include macrophage/microglia activation, astrocytosis and neuronal dysfunction or death. As the molecular mechanisms of this process are poorly understood, we used Atlas human cytokine or cytokine receptor microarray analysis to highlight gene expression profiles that accompanied encephalitis in Simian human immunodeficiency virus (SHIV) 89.6P‐infected macaques. Of the 277 genes screened, marked upregulation of monocyte chemoattractant protein‐1, interferon‐inducible peptide IP‐10 and interleukin‐4 were observed specifically in the encephalitic brains. These genes are collectively known to promote macrophage infiltration and activation and virus replication. In contrast, genes regulating neurotrophic functions, such as brain‐derived neurotrophic factor were downregulated. We also found that some of the apoptosis genes were up‐ or down‐regulated. These data provide a comprehensive spectrum of gene expression that underscores the two major clinical manifestations of this unique syndrome: enhanced virus replication in brain macrophages and dystrophic changes in neurons.
ISSN:0047-2565
1600-0684
DOI:10.1034/j.1600-0684.2003.00030.x