Varicella zoster virus vasculopathy: clinical features and pathogenesis
1Department of Neurology, University of Colorado School of Medicine, 12700 E. 19th Avenue, Mail Stop B182, Aurora, CO, 80045, USA, maria.nagel@ucdenver.edu.
Journal of Neurovirology
|August 7, 2013
Summary
Varicella zoster virus (VZV) vasculopathy involves brain artery inflammation and remodeling, leading to stroke. Diagnosis relies on detecting anti-VZV IgG in cerebrospinal fluid (CSF).
Area of Science:
- Neurology
- Infectious Diseases
- Vascular Biology
Background:
- Varicella zoster virus (VZV) can cause vasculopathy in cerebral arteries.
- This condition leads to inflammation, vascular remodeling, and stroke in both immunocompetent and immunocompromised individuals.
- VZV vasculopathy affects both large and small cerebral vessels.
Purpose of the Study:
- To review the clinical features of VZV vasculopathy.
- To explore potential mechanisms of VZV-induced cerebrovascular remodeling and stroke.
Main Methods:
- Review of clinical case studies and pathological findings in VZV vasculopathy.
- Analysis of MRI abnormalities and diagnostic challenges.
- Examination of histological and immunohistochemical data from infected arteries.
Main Results:
- VZV infection starts in the arterial adventitia and spreads transmurally.
- Histological changes include intima thickening, internal elastic lamina disruption, and smooth muscle cell loss.
- Inflammatory cells, including T cells and neutrophils, infiltrate infected arteries, potentially driving remodeling.
Conclusions:
- VZV vasculopathy is a significant cause of stroke, often difficult to diagnose.
- Understanding the mechanisms of VZV-induced vascular remodeling is crucial for effective treatment.
- Cerebrospinal fluid (CSF) anti-VZV IgG detection is the preferred diagnostic test.
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