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

D. Cory Adamson, Brigitte Wildemann, Masayuki Sasaki, Jonathan D. Glass, Justin C. McArthur, Vesselin I. Christov, Ted M. Dawson, Valina L. Dawson

Research output: Contribution to journalArticle

Abstract

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 α 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.

Original languageEnglish (US)
Pages (from-to)1917-1921
Number of pages5
JournalScience
Volume274
Issue number5294
DOIs
StatePublished - Dec 13 1996

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ASJC Scopus subject areas

  • General

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