Journal article
Varicella zoster virus vasculopathy: The expanding clinical spectrum and pathogenesis
Journal of neuroimmunology, Vol.308, pp.112-117
07/15/2017
DOI: 10.1016/j.jneuroim.2017.03.014
PMCID: PMC5489071
PMID: 28335992
Abstract
Varicella zoster virus (VZV) is a ubiquitous, human alphaherpesvirus that produces varicella on primary infection then becomes latent in ganglionic neurons along the entire neuraxis. In elderly and immunocompromised individuals, VZV reactivates and travels along nerve fibers peripherally resulting in zoster. However, VZV can also spread centrally and infect cerebral and extracranial arteries (VZV vasculopathy) to produce transient ischemic attacks, stroke, aneurysm, sinus thrombosis and giant cell arteritis, as well as granulomatous aortitis. The mechanisms of virus-induced pathological vascular remodeling are not fully elucidated; however, recent studies suggest that inflammation and dysregulation of programmed death ligand-1 play a significant role.
Details
- Title: Subtitle
- Varicella zoster virus vasculopathy: The expanding clinical spectrum and pathogenesis
- Creators
- Maria A Nagel - University of Colorado DenverDallas Jones - University of Colorado DenverAnn Wyborny - University of Colorado Denver
- Resource Type
- Journal article
- Publication Details
- Journal of neuroimmunology, Vol.308, pp.112-117
- DOI
- 10.1016/j.jneuroim.2017.03.014
- PMID
- 28335992
- PMCID
- PMC5489071
- NLM abbreviation
- J Neuroimmunol
- ISSN
- 0165-5728
- eISSN
- 1872-8421
- Grant note
- P01 AG032958 / NIA NIH HHS R01 NS094758 / NINDS NIH HHS
- Language
- English
- Date published
- 07/15/2017
- Academic Unit
- Neurology
- Record Identifier
- 9984826360802771
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