When the varicella-zoster virus becomes active again, it can cause inflammation in blood vessels, which is associated with a higher likelihood of stroke or heart attack.
Mechanism
Synthesis from 3 studies
When the chickenpox virus wakes up, it can reach blood vessels and make them inflamed. This inflammation damages the inner lining of the vessels, which causes blood to clot where it shouldn’t. If that clot blocks a vessel going to the brain or heart, it can cause a stroke or heart attack.
Most probable mechanism
When the chickenpox virus wakes up, it travels to blood vessels and causes them to swell and get damaged. This swelling makes it easier for blood clots to form inside the vessels. If a clot blocks a blood vessel in the brain, it can cause a stroke; if it blocks a vessel in the heart, it can cause a heart attack.
Varicella-zoster virus reactivates in sensory ganglia and spreads to vascular endothelial cells via neural or hematogenous routes.
Viral presence in vascular endothelium triggers local immune cell recruitment and cytokine release, causing inflammation of the vessel wall.
Inflammatory damage to the endothelium exposes subendothelial collagen and tissue factor, promoting platelet adhesion and coagulation cascade activation.
Formation of intravascular thrombi occludes cerebral or coronary arteries, leading to ischemic stroke or myocardial infarction.
Evidence from Studies
Supporting (3)
Community contributions welcome
Herpes zoster and the risk of ischemic and hemorrhagic stroke: A systematic review and meta-analysis
Herpes zoster ophthalmicus with associated vasculopathy causing stroke
Varicella Zoster Virus and Stroke: An Intricate Relationship
Contradicting (0)
Community contributions welcome
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