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Developments in Varicella Zoster Virus Vasculopathy.

Maria A Nagel1, Don Gilden2,3

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Area of Science:

  • Neurology
  • Virology
  • Immunology

Background:

  • Varicella zoster virus (VZV), a neurotropic human herpesvirus, causes chickenpox and shingles.
  • VZV establishes latency in neurons and can reactivate, leading to neurological complications like postherpetic neuralgia, meningoencephalitis, myelitis, and vasculopathy, sometimes without a rash.
  • VZV vasculopathy affects both immunocompetent and immunocompromised individuals, including vaccine recipients.

Purpose of the Study:

  • To review the association between VZV and stroke.
  • To discuss the spectrum of disorders caused by VZV vasculopathy.
  • To explore the link between VZV vasculopathy and giant cell arteritis (GCA).

Main Methods:

  • Literature review of clinical-virological case reports.
  • Retrospective pathological-virological analyses of temporal arteries.
  • Focus on VZV infection of cerebral arteries and extracranial VZV vasculopathy.

Main Results:

  • VZV infection of cerebral arteries can lead to ischemic stroke and intracerebral aneurysms, with or without hemorrhage.
  • Extracranial VZV vasculopathy is implicated in triggering the immunopathology of GCA.
  • Prolonged corticosteroid use in GCA may exacerbate VZV infection, leading to fatal vasculopathy.

Conclusions:

  • VZV is a significant cause of stroke and cerebrovascular disease.
  • VZV vasculopathy plays a role in the pathogenesis of GCA.
  • Careful consideration of VZV infection is crucial in managing vasculitic conditions, especially with corticosteroid therapy.