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.

Keywords

Nitric oxide synthaseProinflammatory cytokineImmunologyPathogenesisMicrogliaTumor necrosis factor alphaMediatorDementiaBiologyInflammationMedicineNitric oxidePathologyCell biologyEndocrinologyDisease

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Year
1996
Type
article
Volume
274
Issue
5294
Pages
1917-1921
Citations
419
Access
Closed

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D. Cory Adamson, Brigitte Wildemann, Masayuki Sasaki et al. (1996). Immunologic NO Synthase: Elevation in Severe AIDS Dementia and Induction by HIV-1 gp41. Science , 274 (5294) , 1917-1921. https://doi.org/10.1126/science.274.5294.1917

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DOI
10.1126/science.274.5294.1917