期刊
FRONTIERS IN BIOSCIENCE
卷 13, 期 -, 页码 3913-3918出版社
FRONTIERS IN BIOSCIENCE INC
DOI: 10.2741/2979
关键词
HIV-1; HAD; neurons; astrocytes; macrophages; blood brain barrier; review
资金
- NCRR NIH HHS [P20 RR016443, P20 RR016443-079004, RR016443] Funding Source: Medline
- NIDA NIH HHS [DA020392-01, R01 DA020392-01A1, R01 DA020392] Funding Source: Medline
- NIMH NIH HHS [R01 MH068212-01A1, R03 MH062969-01, MH62969-01, R01 MH068212, R21 MH072355, MH-068212, MH072355] Funding Source: Medline
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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