Immunologic NO synthase: elevation in severe AIDS dementia and induction by HIV-1 gp41.


Journal Article

Indirect mechanisms are implicated in the pathogenesis of the dementia associated with human immunodeficiency virus-type 1 (HIV-1) infection. Proinflammatory molecules such as tumor necrosis factor alpha and eicosanoids are elevated in the central nervous system of patients with HIV-1-related dementia. Nitric oxide (NO) is a potential mediator of neuronal injury, because cytokines may activate the immunologic (type II) isoform of NO synthase (iNOS). The levels of iNOS in severe HIV-1-associated dementia coincided with increased expression of the HIV-1 coat protein gp41. Furthermore, gp41 induced iNOS in primary cultures of mixed rat neuronal and glial cells and killed neurons through a NO-dependent mechanism. Thus, gp41-induced NO formation may contribute to the severe cognitive dysfunction associated with HIV-1 infection.

Full Text

Cited Authors

  • Adamson, DC; Wildemann, B; Sasaki, M; Glass, JD; McArthur, JC; Christov, VI; Dawson, TM; Dawson, VL

Published Date

  • December 1996

Published In

Volume / Issue

  • 274 / 5294

Start / End Page

  • 1917 - 1921

PubMed ID

  • 8943206

Pubmed Central ID

  • 8943206

Electronic International Standard Serial Number (EISSN)

  • 1095-9203

International Standard Serial Number (ISSN)

  • 0036-8075

Digital Object Identifier (DOI)

  • 10.1126/science.274.5294.1917


  • eng