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Update on Varicella Zoster Virus Vasculopathy

  • Central Nervous System Infections (J Lyons, Section Editor)
  • Published:
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Abstract

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.

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Acknowledgments

This work was supported in part by NIH grants AG006127 and AG032958 to D.G. and NS067070 to M.A.N. We thank Marina Hoffman for editorial assistance and Lori DePriest for manuscript preparation.

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Conflict of Interest

Maria A. Nagel received a grant from the NIH. Don Gilden has received grants from the NIH.

Human and Animal Rights and Informed Consent

This article does not contain any studies with human or animal subjects performed by the author.

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Correspondence to Don Gilden.

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This article is part of the Topical Collection on Central Nervous System Infections.

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Nagel, M.A., Gilden, D. Update on Varicella Zoster Virus Vasculopathy. Curr Infect Dis Rep 16, 407 (2014). https://doi.org/10.1007/s11908-014-0407-z

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