Gray F, Adle-Biassette H, Chretien F, Wingertsmann L, Hery C, Tardieu M.
J Neurovirol. 1998 Jun 3-6; 4: 352.
Faculte de Medecine Paris-Ouest, Garches, France.
Neuronal loss has been shown to occur in HIV infection and we and others have shown that it was, at least parltly, due to an apoptotic process [Adle-Biassette, Neuropathol Appl Neurobiol 1995;21:218 - 227]. However, the cause of neuronal damage in HIV infection is still unclear. Productive HIV infection of nerve cells has never been conclusively shown and an indirect mechanism is likely. The neurotoxicity of viral proteins or substances produced by activated glial cells such as cytokines or peroxydes has been postulated. Recently, axonal damage has been demonstrated in the brains of HIV infected patients [Giometto, Ann Neurol 1997;42:34; An, J Neuropathol Exp Neurol 1997;56:1262] and it was proposed that it could play a causative role in neuronal apoptosis. In order to characterize the distribution of apoptotic neurons and their relationships with the stage of the disease, degree of productive HIV infection, microglial activation, peroxyde production and axonal damage, we examined samples of frontal and temporal cortex, basal ganglia and brainstem from 20 patients with AIDS, 20 HIV-positive asymptomatic cases and 10 seronegative controls. Neuronal apoptosis was demonstrated by in situ end labelling in all the AIDS cases and 2 pre-AIDS cases but not in the controls. Semiquantitative evaluation showed that apoptosis was more severe in atrophic brains. It was not directly related to a history of dementia, the expression of HIV protein p24, or to microglial activation judged by the expression of MHC II antigens and cytokines. Significant expression of inductible nitric oxyde synthase and superoxydismutase was only found in 3 brains with HIV encephalitis, interestingly the only 3 cases with a history of dementia. Axonal damage was identified using beta- amyloid-protein precursor immunostaining in 11 AIDS and 1 pre-AIDS brains. Although no quantitative correlation could be established between axonal damage and neuronal apoptosis there was an obvious topographic correlation supporting the view that axonal damage may participate in neuronal apoptosis.
Publication Types:
Keywords:
- AIDS Dementia Complex
- Acquired Immunodeficiency Syndrome
- Amyloid beta-Protein Precursor
- Apoptosis
- Atrophy
- Brain
- Gene Expression
- HIV
- HIV Infections
- Humans
- Microglia
- Neurons
- Neurosciences
- Nitric Oxide Synthase
- Peripheral Nervous System
- Viral Proteins
- genetics
- organization & administration
Other ID:
UI: 102237412
From Meeting Abstracts