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Herpes Simplex Virus 1 Infection Does Not Increase Amyloid-β Pathology in APP/PS1 Mice
Lina Lapeyre1, Jocelyne Piret1, Chantal Rhéaume1
1Research Center in infectious diseases, Research center of the CHU de Québec-Laval University, Quebec City, QC, Canada.
Journal of Alzheimer'S Disease : JAD
|December 25, 2023
Summary
Herpes simplex virus 1 (HSV-1) intranasal infection did not accelerate Alzheimer's disease-like pathology in APP/PS1 mice. Amyloid-beta plaque deposition and related disease markers remained unchanged after HSV-1 infection.
Area of Science:
- Neuroscience
- Virology
- Pathology
Background:
- Investigating the link between herpes simplex virus 1 (HSV-1) infection and Alzheimer's disease (AD) pathology.
- Utilizing APP/PS1 transgenic mice, a model for amyloid-beta (Aβ) deposition characteristic of AD.
- Examining the impact of early-stage HSV-1 infection on AD-like pathology development.
Discussion:
- HSV-1 infection did not significantly alter body weight, clinical symptoms, or survival rates in APP/PS1 mice compared to wild-type controls.
- Analysis revealed no significant differences in amyloid-beta plaque load, microglial activation, or circulating monocyte subsets between infected and non-infected APP/PS1 mice.
- These findings suggest that intranasal HSV-1 infection does not exacerbate or modify established amyloid-beta pathology in this AD mouse model.
Key Insights:
- Early-life intranasal HSV-1 infection does not influence amyloid-beta plaque formation or progression in APP/PS1 mice.
- No acceleration of Alzheimer's disease-like pathology was observed following HSV-1 exposure.
- HSV-1 infection did not impact key AD pathological markers such as amyloid plaques and microglia.
Outlook:
- Further research could explore the effects of different viral strains or infection timings on AD pathology.
- Investigating potential long-term consequences of HSV-1 infection beyond the initial Aβ deposition phase.
- Understanding the complex interplay between viral infections and neurodegenerative diseases is crucial for developing effective therapeutic strategies.
