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Published on: March 16, 2016
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.
Abstract:
Using APP/PS1 mice that overproduce amyloid-β (Aβ) peptides, we investigated whether intranasal infection with a neurovirulent clinical strain of herpes simplex virus 1 (HSV-1) before Aβ deposition could accelerate or increase Alzheimer's disease-like pathology. After HSV-1 infection, APP/PS1 mice presented a similar disease as wild type animals based on body weight changes, clinical symptoms, and survival rates. The number and volume of Aβ plaques, the number of microglia, and the percentages of circulating monocyte subsets were similar in APP/PS1 mice infected or not with HSV-1. Thus, intranasal infection with HSV-1 does not alter Aβ pathology in this mouse model.
Insights
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.
