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Review
. 2017 Jul 15:308:112-117.
doi: 10.1016/j.jneuroim.2017.03.014. Epub 2017 Mar 18.

Varicella zoster virus vasculopathy: The expanding clinical spectrum and pathogenesis

Maria A Nagel  1 , Dallas Jones  2 , Ann Wyborny  3
Affiliations
Review

Varicella zoster virus vasculopathy: The expanding clinical spectrum and pathogenesis

Maria A Nagel et al. J Neuroimmunol. .

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.

Keywords: Aortitis; Giant cell arteritis; Inflammation; Stroke; Varicella zoster virus; Vasculopathy.

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Conflict of interest statement

Statement of interest

The authors declare no conflict of interest.

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