Influence of HAART on HIV-related CNS disease and neuroinflammation

I C Anthony, S N Ramage, F W Carnie, P Simmonds, J E Bell

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

Neuroinflammation has an established link with AIDS-related dementia but has not been investigated in the post-highly active anti-retroviral therapy (HAART) era. In this autopsy study we examined post-HAART cases in Edinburgh for the presence of HIV-related pathology and in well-treated cases for evidence of neuroinflammation. We focused on basal ganglia and the hippocampus, 2 key areas of the brain for cognitive functioning and compared pre- and post-HAART cases for neuroinflammatory status. We find evidence, post-HAART, that there is a high level of microglial/macrophage activation that is comparable with the levels seen, pre-HAART, in HIV encephalitis (HIVE) and AIDS cases. This result was maximal in the hippocampus where microglial/macrophage upregulation in the HAART-treated group exceeded that seen in HIVE. In the basal ganglia, HAART-treated cases showed significantly higher levels of CD68-positive microglia/macrophages than in control brains (p = 0.004), and in the hippocampus levels were significantly higher than those seen in control cases, pre-HAART AIDS, and presymptomatic brains (p = 0.01). However, lymphocyte levels in the areas examined were low in HAART-treated cases. We conclude that there is a surprising degree of ongoing neuroinflammation in HAART-treated patients, particularly in the hippocampus. This may pose a threat for the future health of individuals maintained long-term on HAART therapy.
Original languageEnglish
Pages (from-to)529-36
Number of pages8
JournalJournal of Neuropathology & Experimental Neurology
Volume64
Issue number6
Publication statusPublished - Jun 2005

Keywords / Materials (for Non-textual outputs)

  • Acquired Immunodeficiency Syndrome
  • Adolescent
  • Adult
  • Antigens, CD
  • Antiretroviral Therapy, Highly Active
  • Brain
  • Central Nervous System Diseases
  • Female
  • Glial Fibrillary Acidic Protein
  • Humans
  • Immunohistochemistry
  • Inflammation
  • Ki-67 Antigen
  • Male
  • Middle Aged

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