Update on varicella zoster virus vasculopathy
Nagel, M.A.; Gilden, D.
Current Infectious Disease Reports 16(6): 407
2014
ISSN/ISBN: 1523-3847
PMID: 24819870
DOI: 10.1007/s11908-014-0407-z
Accession: 056777690
Primary infection of humans with varicella zoster virus (VZV) causes varicella (chickenpox), after which the virus becomes latent in cranial nerve ganglia, dorsal root ganglia and autonomic ganglia along the entire neuraxis. As VZV-specific cell-mediated immunity declines in elderly and immunocompromised individuals, VZV reactivates from one or more ganglia and typically causes herpes zoster (shingles). Zoster may also be complicated by VZV vasculopathy due to productive virus infection of the cerebral arteries. In recent decades, the clinical spectrum of VZV vasculopathy has expanded to include not only transient ischemic attacks and ischemic and hemorrhagic stroke, but also multifocal VZV vasculopathy, with temporal artery infection mimicking giant cell arteritis, extracranial vasculopathy, aneurysm with and without subarachnoid hemorrhage, arterial dissection and dolichoectasia, ischemic cranial neuropathies, cerebral venous sinus thrombosis, spinal cord infarction and peripheral thrombotic disease.