Journal
JOURNAL OF NEUROSCIENCE
Volume 27, Issue 47, Pages 12844-12850Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.4154-07.2007
Keywords
neuroinflammation; NeuroAIDS; apoptosis; chemokines; CCL2/ MCP-1; Connexin
Categories
Funding
- NIAID NIH HHS [AI-051519, P30 AI051519] Funding Source: Medline
- NIMH NIH HHS [MH070297, MH075679, K01 MH076679, R01 MH070297, K01 MH076679-01A1, K01 MH076679-02, R01 MH075679] Funding Source: Medline
- NINDS NIH HHS [NS11920, P50 NS011920] Funding Source: Medline
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Human immunodeficiency virus (HIV) entry into the CNS is an early event after infection, resulting in neurological dysfunction in a significant number of individuals. As people with acquired immunodeficiency syndrome ( AIDS) live longer, the prevalence of cognitive impairment is increasing, despite antiretroviral therapy. The mechanisms that mediate CNS dysfunction are still not completely understood, and include inflammation, viral presence, and/or replication. In this report, we characterize a novel role of gap junctions in transmitting and thereby amplifying toxic signals originating from HIV-infected astrocytes that trigger cell death in uninfected astrocytes. HIV-infected astrocytes were resistant to apoptosis; however, uninfected astrocytes forming gap junctions with infected astrocytes were apoptotic. Gap junction blockers abolished apoptosis in uninfected astrocytes, supporting the role of these channels in amplifying cell death. Our findings describe a novel mechanism of toxicity within the brain, triggered by low numbers of HIV-infected astrocytes and amplified by gap junctions, contributing to the pathogenesis of NeuroAIDS.
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