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Zoster-Associated Prothrombotic Plasma Exosomes and Increased Stroke Risk
Andrew N Bubak1, Christina Coughlan1, Janelle Posey2
1Department of Neurology, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA.
The Journal of Infectious Diseases
|October 6, 2022
Summary
Herpes zoster (shingles) reactivation elevates stroke risk. Shingles-derived exosomes promote blood clotting and inflammation, potentially explaining this increased risk and suggesting new prevention strategies.
Area of Science:
- Virology
- Immunology
- Neurology
- Cardiovascular Science
Background:
- Herpes zoster (HZ), or shingles, is caused by varicella zoster virus reactivation.
- HZ increases stroke risk for up to one year post-infection, but mechanisms remain unclear.
- The occurrence of distant strokes suggests a persistent, virus-induced soluble factor.
Purpose of the Study:
- To investigate the role of circulating plasma exosomes in HZ-associated stroke risk.
- To analyze the protein content and functional effects of exosomes from HZ patients.
Main Methods:
- Collected and analyzed plasma exosomes from patients with and without HZ.
- Assessed exosome protein content for prothrombotic factors.
- Evaluated exosome-induced activation of platelets and formation of platelet-leukocyte aggregates.
- Tested exosome effects on cerebrovascular cells, measuring cytokine secretion.
Main Results:
- HZ exosomes contain proteins that induce a prothrombotic state in recipient cells.
- HZ exosomes activate platelets, leading to platelet-leukocyte aggregate formation.
- Exosomes from patients 3 months post-HZ also triggered pro-inflammatory cytokine (IL-6, IL-8) secretion by cerebrovascular cells.
Conclusions:
- Circulating exosomes from HZ patients contribute to a prothrombotic and pro-inflammatory state.
- These findings suggest a mechanism linking HZ to increased stroke risk.
- Potential clinical implications include using antiplatelet agents and increasing HZ vaccination.
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