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Neuropathology of early HIV-1 infection

Neuropathology of early HIV-1 infection
Neuropathology of early HIV-1 infection

Early HIV-1 invasion of the central nervous system has been demonstrated by many cerebrospinal fluid studies; however, most HIV-1 carriers remain neurologically unimpaired during the so called 'asymptomatic' period lasting from seroconversion to symptomatic AIDS. Therefore, neuropathological studies in the early pre-AIDS stages are very few, and the natural history of central nervous system changes in HIV-1 infection remains poorly understood. Examination of brains of asymptomatic HIV-1 positive individuals who died accidentally and of rare cases with acute fatal encephalopathy revealing HIV infection, and comparison with experimental simian immunodeficiency virus and feline immunodeficiency virus infections suggest that, invasion of the CNS by HIV-1 occurs at the time of primary infection and induces an immunological process in the central nervous system. This includes an inflammatory T-cell reaction with vasculitis and leptomeningitis, and immune activation of brain parenchyma with increased number of microglial cells, upregulation of major histocompatibility complex class II antigens and local production of cytokines. Myelin pallor and gliosis of the white matter are usually found and are likely to be the consequence of opening of the blood brain barrier due to vasculitis; direct damage to oligodendrocytes by cytokines may also interfere. These white matter changes may explain, at least partly, the early cerebral atrophy observed, by magnetic resonance imaging, in asymptomatic HIV-1 carriers. In contrast, cortical damage seems to be a late event in the course of HIV-1 infection. There it; no significant neuronal loss at the early stages of the disease, no accompanying increase in glial fibrillary acid protein staining in the cortex, and only exceptional neuronal apoptosis. Although HIV-1 proviral DNA may be demonstrated in a number of brains, viral replication remains very low during the asymptomatic stage of HIV-1 infection. This makes it likely that, although opening of the blood brain barrier may facilitate viral entry into the brain, specific immune responses including both neutralising antibodies and cytotoxic T-lymphocytes, continuously inhibits viral replication at that stage.

1015-6305
1-15
Gray, Françoise
863ce1c9-7cfa-49be-88c1-5534bf45991e
Scaravilli, Francesco
b4a19914-da47-4461-b78d-7bf5690a8ea7
Everall, Ian
7e01f0fa-3c04-41db-a2c3-9e04678b192e
Chretien, Fabrice
3e9f581a-13f1-42e0-886c-bbff876133c2
An, Shu
2f3f0eeb-da8a-4a66-b765-ed8cf761dfdd
Boche, Delphine
bdcca10e-6302-4dd0-919f-67218f7e0d61
Adle-Biassette, Homa
7d01b035-7e20-4ee7-afda-88579e3dc92c
Wingertsmann, Laure
b8b9dcca-5f11-44e7-9ef2-ce80229fa35a
Durigon, Michel
48440229-5aa1-4770-b2b0-f311a869094c
Hurtrel, Bruno
6798d5fc-3ad6-431f-89d7-f269f9a17c4f
Chiodi, Francesca
76179e57-19de-43f5-90d7-402e6156d72c
Bell, Jeanne
b885fa70-7be8-4990-bdbb-989681746817
Lantos, Peter
b11df872-5b67-4df1-bc1e-3e204eaca995
Gray, Françoise
863ce1c9-7cfa-49be-88c1-5534bf45991e
Scaravilli, Francesco
b4a19914-da47-4461-b78d-7bf5690a8ea7
Everall, Ian
7e01f0fa-3c04-41db-a2c3-9e04678b192e
Chretien, Fabrice
3e9f581a-13f1-42e0-886c-bbff876133c2
An, Shu
2f3f0eeb-da8a-4a66-b765-ed8cf761dfdd
Boche, Delphine
bdcca10e-6302-4dd0-919f-67218f7e0d61
Adle-Biassette, Homa
7d01b035-7e20-4ee7-afda-88579e3dc92c
Wingertsmann, Laure
b8b9dcca-5f11-44e7-9ef2-ce80229fa35a
Durigon, Michel
48440229-5aa1-4770-b2b0-f311a869094c
Hurtrel, Bruno
6798d5fc-3ad6-431f-89d7-f269f9a17c4f
Chiodi, Francesca
76179e57-19de-43f5-90d7-402e6156d72c
Bell, Jeanne
b885fa70-7be8-4990-bdbb-989681746817
Lantos, Peter
b11df872-5b67-4df1-bc1e-3e204eaca995

Gray, Françoise, Scaravilli, Francesco, Everall, Ian, Chretien, Fabrice, An, Shu, Boche, Delphine, Adle-Biassette, Homa, Wingertsmann, Laure, Durigon, Michel, Hurtrel, Bruno, Chiodi, Francesca, Bell, Jeanne and Lantos, Peter (1996) Neuropathology of early HIV-1 infection. Brain Pathology, 6 (1), 1-15. (doi:10.1111/j.1750-3639.1996.tb00775.x).

Record type: Review

Abstract

Early HIV-1 invasion of the central nervous system has been demonstrated by many cerebrospinal fluid studies; however, most HIV-1 carriers remain neurologically unimpaired during the so called 'asymptomatic' period lasting from seroconversion to symptomatic AIDS. Therefore, neuropathological studies in the early pre-AIDS stages are very few, and the natural history of central nervous system changes in HIV-1 infection remains poorly understood. Examination of brains of asymptomatic HIV-1 positive individuals who died accidentally and of rare cases with acute fatal encephalopathy revealing HIV infection, and comparison with experimental simian immunodeficiency virus and feline immunodeficiency virus infections suggest that, invasion of the CNS by HIV-1 occurs at the time of primary infection and induces an immunological process in the central nervous system. This includes an inflammatory T-cell reaction with vasculitis and leptomeningitis, and immune activation of brain parenchyma with increased number of microglial cells, upregulation of major histocompatibility complex class II antigens and local production of cytokines. Myelin pallor and gliosis of the white matter are usually found and are likely to be the consequence of opening of the blood brain barrier due to vasculitis; direct damage to oligodendrocytes by cytokines may also interfere. These white matter changes may explain, at least partly, the early cerebral atrophy observed, by magnetic resonance imaging, in asymptomatic HIV-1 carriers. In contrast, cortical damage seems to be a late event in the course of HIV-1 infection. There it; no significant neuronal loss at the early stages of the disease, no accompanying increase in glial fibrillary acid protein staining in the cortex, and only exceptional neuronal apoptosis. Although HIV-1 proviral DNA may be demonstrated in a number of brains, viral replication remains very low during the asymptomatic stage of HIV-1 infection. This makes it likely that, although opening of the blood brain barrier may facilitate viral entry into the brain, specific immune responses including both neutralising antibodies and cytotoxic T-lymphocytes, continuously inhibits viral replication at that stage.

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Published date: 1 January 1996

Identifiers

Local EPrints ID: 438810
URI: http://eprints.soton.ac.uk/id/eprint/438810
ISSN: 1015-6305
PURE UUID: fa066f95-5263-409a-8f90-c95a835733a0
ORCID for Delphine Boche: ORCID iD orcid.org/0000-0002-5884-130X

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Date deposited: 24 Mar 2020 17:52
Last modified: 27 Apr 2022 01:42

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Contributors

Author: Françoise Gray
Author: Francesco Scaravilli
Author: Ian Everall
Author: Fabrice Chretien
Author: Shu An
Author: Delphine Boche ORCID iD
Author: Homa Adle-Biassette
Author: Laure Wingertsmann
Author: Michel Durigon
Author: Bruno Hurtrel
Author: Francesca Chiodi
Author: Jeanne Bell
Author: Peter Lantos

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