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Jenae Limoges, Yuri Persidsky, Paul Bock, Howard E. Gendelman, Dexamethasone Therapy Worsens the Neuropathology of Human Immunodeficiency Virus Type 1 Encephalitis in SCID Mice, The Journal of Infectious Diseases, Volume 175, Issue 6, June 1997, Pages 1368–1381, https://doi.org/10.1086/516469
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Abstract
Humanimmunodeficiency virus (HIV) dementia is a late complicationof viral infection. Cognitive dysfunction revolves around the secretion of neurotoxins from immunologically competent virus-infected brain macrophages and microglia. Such macrophage neurotoxins are inflammatory factors that produce selective neuronal dysfunction and ultimately cell death. To evaluate the potential efficacy of antiinflammatory therapy for HIV dementia, dexamethasone was administered to severe combined immunodeficient mice with HIV-1 encephalitis. Mice were given therapeutic doses of dexamethasone before intracerebral inoculation with HIV-1-infected human monocytes. Histochemical evaluation showed a worsening of neuropathology after treatment, with astrogliosis and increased apoptosis of neurons. Laboratory investigation of the mechanisms for the dexamethasone effects revealed increased viability of HIV-infected macrophages and incomplete suppression of neurotoxic inflammatory secretions . The results suggest the need for caution in administering glucocorticoids for treatment of HIV encephalitis in humans.
- apoptosis
- hiv
- encephalitis
- aids dementia complex
- dementia
- dexamethasone
- glucocorticoids
- bodily secretions
- cell death
- hiv-1
- macrophages
- scid mice
- microglia
- monocytes
- neurons
- neurotoxins
- vaccination
- virus diseases
- brain
- mice
- viruses
- cognitive impairment
- hiv encephalopathy
- hiv infections
- neuropathology