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Viral load and neuropathology in the SIV model

Viral load and neuropathology in the SIV model
Viral load and neuropathology in the SIV model

To investigate neuropathological processes involved in HIV infection, a longitudinal analysis of central nervous system (CNS) changes was performed using the SIV-infected macaque model. Five animals were studied during the early phase and 13 during the asymptomatic and symptomatic phases. Histopathological analyses were performed on one cerebral fixed hemisphere whereas on the other frozen hemisphere in situ hybridisation, immunohistochemistry and RT-PCR were performed. Viral load was quantified by in situ hybridisation, CD4 and CD8 T cell infiltration by immunohistochemistry and mRNA cytokine expression (IL1β, IL2, IL6, TNFα, IFNγ and TGF-β1) by semiquantitative RT-PCR. As reported for HIV-infected humans, the neuropathological analysis of SIV infected animals revealed four distinct lesion profiles: minimal changes, early encephalitis, leukoencephalopathy and encephalitis. No relationship was found between neuropathological findings, numbers of SIV replicating cells and T cell infiltration. CNS infection was found to be an early event characterised by glial activation, an increase in the level of IL1β, TNFα and IL6 mRNA expression. During the asymptomatic and symptomatic phases, IL6 and IL1β mRNAs increase coincided with gliosis and the development of myelin lesions. The absence of relationship between neuropathological findings and viral load suggests that cerebral lesions are caused by an indirect mechanism. Inflammatory cytokine pattern associated with severe lesions show the key role of glial activation in the SIV neuropathological process.

Cytokines, Lymphocyte T infiltration, Neuropathology, SIV
1355-0284
232-240
Boche, D.
bdcca10e-6302-4dd0-919f-67218f7e0d61
Khatissian, E.
616c1ecd-d182-435a-a315-05c8e9faf22d
Gray, F.
863ce1c9-7cfa-49be-88c1-5534bf45991e
Falanga, P.
513a8f36-e98f-4a0f-bd46-c1177114faa6
Montagnier, L.
80c2ecb7-a62e-4b81-a1dd-5438bc61f05f
Hurtrel, B.
6798d5fc-3ad6-431f-89d7-f269f9a17c4f
Boche, D.
bdcca10e-6302-4dd0-919f-67218f7e0d61
Khatissian, E.
616c1ecd-d182-435a-a315-05c8e9faf22d
Gray, F.
863ce1c9-7cfa-49be-88c1-5534bf45991e
Falanga, P.
513a8f36-e98f-4a0f-bd46-c1177114faa6
Montagnier, L.
80c2ecb7-a62e-4b81-a1dd-5438bc61f05f
Hurtrel, B.
6798d5fc-3ad6-431f-89d7-f269f9a17c4f

Boche, D., Khatissian, E., Gray, F., Falanga, P., Montagnier, L. and Hurtrel, B. (1999) Viral load and neuropathology in the SIV model. Journal of Neurovirology, 5 (3), 232-240. (doi:10.3109/13550289909015809).

Record type: Article

Abstract

To investigate neuropathological processes involved in HIV infection, a longitudinal analysis of central nervous system (CNS) changes was performed using the SIV-infected macaque model. Five animals were studied during the early phase and 13 during the asymptomatic and symptomatic phases. Histopathological analyses were performed on one cerebral fixed hemisphere whereas on the other frozen hemisphere in situ hybridisation, immunohistochemistry and RT-PCR were performed. Viral load was quantified by in situ hybridisation, CD4 and CD8 T cell infiltration by immunohistochemistry and mRNA cytokine expression (IL1β, IL2, IL6, TNFα, IFNγ and TGF-β1) by semiquantitative RT-PCR. As reported for HIV-infected humans, the neuropathological analysis of SIV infected animals revealed four distinct lesion profiles: minimal changes, early encephalitis, leukoencephalopathy and encephalitis. No relationship was found between neuropathological findings, numbers of SIV replicating cells and T cell infiltration. CNS infection was found to be an early event characterised by glial activation, an increase in the level of IL1β, TNFα and IL6 mRNA expression. During the asymptomatic and symptomatic phases, IL6 and IL1β mRNAs increase coincided with gliosis and the development of myelin lesions. The absence of relationship between neuropathological findings and viral load suggests that cerebral lesions are caused by an indirect mechanism. Inflammatory cytokine pattern associated with severe lesions show the key role of glial activation in the SIV neuropathological process.

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More information

Accepted/In Press date: 24 November 1998
Published date: 1 January 1999
Keywords: Cytokines, Lymphocyte T infiltration, Neuropathology, SIV

Identifiers

Local EPrints ID: 438025
URI: http://eprints.soton.ac.uk/id/eprint/438025
ISSN: 1355-0284
PURE UUID: 45b98909-f2ba-448d-b9a7-9babcbc32687
ORCID for D. Boche: ORCID iD orcid.org/0000-0002-5884-130X

Catalogue record

Date deposited: 26 Feb 2020 17:31
Last modified: 07 Oct 2020 01:44

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