Human immunodeficiency virus infection, inducible nitric oxide synthase expression, and microglial activation: Pathogenetic relationship to the acquired immunodeficiency syndrome dementia complex

Kevin Rostasy, Laura Monti, Constantin Yiannoutsos, Michelle Kneissl, Jeanne Bell, Thomas L. Kemper, John C. Hedreen, Bradford A. Navia

Research output: Contribution to journalArticle

72 Scopus citations


The regional expression of immune-mediated and neurotoxic events in the human immunodeficiency virus (HIV)infected brain in relationship to the acquired immunodeficiency syndrome (AIDS) dementia complex (ADC) and brain pathology remains uncertain. The extent of gp41, inducible nitric oxide synthase (iNOS), and HLA-DR expression was examined in the frontal lobe and basal ganglia of 25 patients at varying stages of ADC. The expression of gp41 and iNOS was present predominantly in perivascular cells and most often in the basal ganglia. Staining for gp41 correlated significantly with iNOS in the basal ganglia, whereas the severity of staining for gp41 and iNOS in the basal ganglia and white matter was significantly greater in subjects with moderate to severe dementia compared with those with milder impairment. The degree of macrophage staining in the white matter and basal ganglia also correlated significantly with ADC severity and was more abundant than gp41 or iNOS staining, particularly in the white matter. Logistic regression analysis revealed that staining for iNOS and gp41 increased linearly with ADC severity and was significantly more abundant in the basal ganglia compared with the white matter. Double-immunolabeling studies colocalized iNOS predominantly to macrophage/microglia and to gp41-positive cells. The expression of iNOS and gp41 in the basal ganglia combined with immune activation contributes to the development and progression of the clinical syndrome.

Original languageEnglish (US)
Pages (from-to)207-216
Number of pages10
JournalAnnals of Neurology
Issue number2
StatePublished - Aug 23 1999


ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

Cite this