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Human immunodeficiency virus encephalitis in SCID mice

Y Persidsky¹, J Limoges, R McComb

¹Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha 68198-5215, USA.

The American Journal of Pathology

|September 1, 1996

Summary

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A new severe combined immunodeficiency (SCID) mouse model using human immunodeficiency virus (HIV)-infected monocytes shows promise for studying HIV dementia. This model replicates key neuropathological features, aiding therapeutic development for cognitive and motor deficits.

Area of Science:

Neuroscience
Immunology
Virology

Background:

Human immunodeficiency virus (HIV) infection can lead to neuroinvasion and cognitive/motor deficits, known as HIV dementia.
The pathogenesis of HIV dementia involves secretory products from immune-activated brain macrophages and microglia.

Purpose of the Study:

To develop and validate an animal model for quantitatively evaluating HIV-induced neuropathology.
To assess the utility of a SCID mouse model with xenografts of HIV-1-infected cells for studying HIV dementia.

Main Methods:

Xenografts of HIV-1-infected human monocytes were inoculated into the brains of SCID mice.
HIV-1 p24 antigen expression, inflammatory responses (astrogliosis, cytokine production), microglial activation, and neuronal injury were quantitatively evaluated.

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Main Results:

HIV-1-infected monocyte xenografts remained viable and expressed HIV-1 p24 antigen persistently in mouse brains.
Progressive inflammatory responses, including astrogliosis and microglial activation (IL-1 beta, IL-6), were observed.
Neuronal injury (apoptosis) and an inflammatory reaction in human monocytes (HLA-DR, IL-1 beta, IL-6, TNF-alpha) were detected.

Conclusions:

The SCID mouse model successfully reproduces key aspects of HIV-1 neuropathogenesis, including infected macrophages, astrocytosis, microglial activation, and neuronal damage.
This model serves as a valuable tool for developing therapeutics to improve cognitive and motor function in HIV-infected individuals.