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A Thin-skull Window Technique for Chronic Two-photon In vivo Imaging of Murine Microglia in Models of Neuroinflammation
Published on: September 19, 2010
Gradient of microglial activation in the brain of SIV infected macaques
N E Berman1, L G Sheffield, J Purcell
1Department of Anatomy and Cell Biology, University of Kansas Medical Center, 3901 Rainbow Boulevard, Room 2000 WHE, Kansas City, KS 66160-7400, USA. Nberman@KUMC.edu
Abstract:
Brains of macaques inoculated with macrophage-tropic, neurovirulent virus 7F, with lymphocyte-tropic SIV mac239, or with dual-tropic SIVmac239/1yE, were examined for microglial activation, astrocyte activation, apoptosis and neuron loss. The brain one animal inoculated with neurovirulent virus 7f showed massive microglial activation as assessed by expression of the major histo-compatibility complex class II (MHC-II). In this animal very numerous, large microglial nodules expressing MHC-II were concentrated in the basal pons and internal capsule. These microglial nodules contained cells undergoing apoptosis detected by in situ end labeling of fragmented DNA. In this animal, neuron loss was apparent near the microglial nodules. In the animals inoculated with SIVmac239 or SIVmac239/17E, pathologic changes such as perivascular cuffing and formation of microglial nodules were absent. However, increased expression of MHC-11 by microglial cells was also concentrated in white matter of the basal pons, midbrain and internal capsule. These results indicate the microglial activation in SIV-infected macaques follows a ventral to dorsal gradient regardless of viral tropism. These results also show that the type and severity of neuropathological changes in SIV-infected macaques is highly dependent on the tropism of the inoculated virus.
Insights
Neurovirulent simian immunodeficiency virus (SIV) causes severe brain damage in macaques, including microglial activation and neuron loss. Viral tropism dictates the type and severity of neuropathology in SIV-infected macaques.
Area of Science:
- Neurovirology
- Immunology
- Neuropathology
Background:
- Simian immunodeficiency virus (SIV) infection in macaques serves as a model for human immunodeficiency virus (HIV) encephalitis.
- Understanding the neuropathogenesis of SIV is crucial for developing effective treatments for HIV-associated neurocognitive disorders.
Purpose of the Study:
- To investigate the effects of different SIV strains with varying tropisms on the macaque brain.
- To characterize microglial activation, astrocyte activation, apoptosis, and neuron loss in response to SIV infection.
Main Methods:
- Brains of macaques inoculated with macrophage-tropic, neurovirulent virus 7F, lymphocyte-tropic SIVmac239, or dual-tropic SIVmac239/17E were examined.
- Microglial activation was assessed by major histo-compatibility complex class II (MHC-II) expression.
- Apoptosis was detected using in situ end labeling of fragmented DNA.
Main Results:
- Neurovirulent virus 7F caused massive microglial activation, microglial nodules with apoptosis, and neuron loss, primarily in the basal pons and internal capsule.
- SIVmac239 and SIVmac239/17E infections showed absent perivascular cuffing and microglial nodules, but increased MHC-II expression in white matter.
- Microglial activation followed a ventral to dorsal gradient irrespective of viral tropism.
Conclusions:
- The tropism of the inoculated SIV strain significantly influences the type and severity of neuropathological changes.
- Neurovirulent SIV strains induce more severe neuropathology, including apoptosis and neuron loss, compared to non-neurovirulent strains.
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