Microglia in human disease, with an emphasis on acquired immune deficiency syndrome

D. W. Dickson, L. A. Mattiace, K. Kure, K. Hutchins, W. D. Lyman, C. F. Brosnan

Research output: Contribution to journalReview articlepeer-review

266 Scopus citations


In conclusion, there is overwhelming evidence that within the CNS the primary sites of active HIV-1 infection are microglia. CNS infection may be related to the normal repopulation of the CNS by monocytes (microglial turnover) that carry latent infection into the CNS. Activation of viral infection may depend upon microglial differentiation, soluble factors (cytokines), and/or coexistent infections. Infection of microglia may disturb the normal hemostatic balance that exists between microglia and other glia, and between microglia and neurons, processes that are only recently being explored at the molecular level. The impact that HIV infection of microglia may have on synaptic integrity is unknown. Cytokines appear to be prime candidates as mediators of some of the adverse effects of microglial infection on other CNS cells, myelin and endothelial cells.

Original languageEnglish (US)
Pages (from-to)135-156
Number of pages22
JournalLaboratory Investigation
Issue number2
StatePublished - 1991

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Molecular Biology
  • Cell Biology


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