Varicella zoster virus vasculopathy: The expanding clinical spectrum and pathogenesis.
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.
Department of Neurology, University of Colorado School of Medicine, Aurora, CO 80045, USA. Electronic address: maria.nagel@ucdenver.edu.
Maria A
MA
Nagel
Department of Neurology, University of Colorado School of Medicine, Aurora, CO 80045, USA. Electronic address: dallas.jones@ucdenver.edu.
Dallas
D
Jones
Department of Neurology, University of Colorado School of Medicine, Aurora, CO 80045, USA. Electronic address: ann.wyborny@ucdenver.edu.
Ann
A
Wyborny
D000818:Animals; D002644:Chickenpox / Q000150:complications / Q000276:immunology / Q000821:virology; D006562:Herpes Zoster / Q000150:complications / Q000276:immunology / Q000821:virology; D014645:Herpesvirus 3, Human / Q000472:pathogenicity*; D006801:Humans; D020521:Stroke / Q000209:etiology* / Q000821:virology
Aortitis; Giant cell arteritis; Inflammation; Stroke; Varicella zoster virus; Vasculopathy