ArticleNeurology2011
Varicella zoster virus vasculopathy: analysis of virus-infected arteries.
Article in Neurology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers, 2 of them syntheses that pooled it.
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Who cites it
111 citing papers in PubMed, 2 syntheses or guidelines pooled it, 176 citations in OpenAlex.
- A meta-analysis of stroke risk following herpes zoster infection.BMC infectious diseases · 2017Pooled it
- A systematic review and meta-analysis on herpes zoster and the risk of cardiac and cerebrovascular events.PloS one · 2017Pooled it
- Fulminant varicella-zoster virus meningoencephalitis without rash: Aggressive perivascular necrotizing and leptomeningeal MRI findings.Radiology case reports · 2026Article
- Varicella zoster virus infection.Nature reviews. Disease primers · 2026Review
- Rashless varicella-zoster virus encephalitis diagnosed by metagenomic next-generation sequencing: two case reports.BMC neurology · 2026Article
- A case report of shingles and subsequent cardiac ischaemia in a young male.European heart journal. Case reports · 2026Article
- Varicella zoster virus and the central nervous system.Nature reviews. Microbiology · 2026Review
- Cutaneous Small Vessel Vasculitis Associated With Varicella Zoster Infection: A Case Report and Review of the Literature.International journal of surgical pathology · 2026Review
- Non-neuronal sites of latency for alphaherpesviruses.Journal of virology · 2026Review
- Vertebral Artery Stump Syndrome Caused by Varicella-zoster Virus Vasculopathy in the Absence of a Skin Rash.Internal medicine (Tokyo, Japan) · 2026Article
- Varicella Zoster Virus Infection: Clinical Features, Molecular Pathogenesis, Treatment, and Prevention.MedComm · 2026Review
- Herpes zoster vaccination and incident dementia in Canada: an analysis of natural experiments.The Lancet. Neurology · 2026Article
- Hutchinson's sign complicated by bilateral multiple cranial neuropathies and cerebral infarctions: a case report.Frontiers in medicine · 2026Article
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- Hemichorea as a primary manifestation of varicella-zoster virus neuroinfection in a child - a case report and review of literature.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Review
- A Diagnostic Approach to VZV Vasculopathy Using MR Vessel Wall Imaging.Internal medicine (Tokyo, Japan) · 2025Article
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- Detection of Varicella Zoster Virus Reactivation in Cerebrospinal Fluid in Ischemic Stroke or Transient Ischemic Attack.Journal of the American Heart Association · 2025Article
- Article
- Article
51 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 1 institution in 1 country.
Funding
Abstract
objectiveVaricella zoster virus (VZV) is an under-recognized yet treatable cause of stroke. No animal model exists for stroke caused by VZV infection of cerebral arteries. Thus, we analyzed cerebral and temporal arteries from 3 patients with VZV vasculopathy to identify features that will help in diagnosis and lead to a better understanding of VZV-induced vascular remodeling.
methodsNormal and VZV-infected cerebral and temporal arteries were examined histologically and by immunohistochemistry using antibodies directed against VZV, endothelium, and smooth muscle actin and myosin.
resultsAll VZV-infected arteries contained 1) a disrupted internal elastic lamina; 2) a hyperplastic intima composed of cells expressing α-smooth muscle actin (α-SMA) and smooth muscle myosin heavy chain (SM-myosin) but not endothelial cells expressing CD31; and 3) decreased medial smooth muscle cells. The location of VZV antigen, degree of neointimal thickening, and disruption of the media were related to the duration of disease.
conclusionsThe presence of VZV primarily in the adventitia early in infection and in the media and intima later supports the notion that after reactivation from ganglia, VZV spreads transaxonally to the arterial adventitia followed by transmural spread of virus. Disruption of the internal elastic lamina, progressive intimal thickening with cells expressing α-SMA and SM-MHC, and decreased smooth muscle cells in the media are characteristic features of VZV vasculopathy. Stroke in VZV vasculopathy may result from changes in arterial caliber and contractility produced in part by abnormal accumulation of smooth muscle cells and myofibroblasts in thickened neointima and disruption of the media.
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Registered trials
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