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Area of Science:

  • Neuroscience
  • Infectious Diseases
  • Vascular Biology

Background:

  • Varicella zoster virus (VZV) establishes latency in neurons post-primary infection (chickenpox).
  • Reactivation of VZV causes herpes zoster (shingles), particularly in immunocompromised individuals.
  • Emerging evidence links VZV to cerebrovascular disease, termed VZV vasculopathy.

Purpose of the Study:

  • To review the history, clinical features, and mechanisms of VZV vasculopathy.
  • To discuss epidemiological studies linking zoster to stroke risk.
  • To explore the potential benefits of antiviral therapy in reducing stroke risk post-zoster.

Main Methods:

  • Review of case reports and clinical findings related to VZV vasculopathy.
  • Analysis of large-scale epidemiological studies from Taiwan, Denmark, and the UK.
  • Discussion of proposed pathophysiological mechanisms of VZV-induced stroke.

Main Results:

  • VZV infection of cerebral arteries can directly cause pathological vascular remodeling and stroke.
  • Epidemiological data confirm zoster as a significant risk factor for stroke.
  • Antiviral therapy has shown potential in reducing the stroke risk associated with zoster.

Conclusions:

  • VZV vasculopathy is a recognized cause of stroke, particularly following zoster reactivation.
  • Zoster significantly increases the risk of stroke, necessitating awareness and preventative strategies.
  • Antiviral treatment may be a crucial intervention to prevent stroke in zoster patients.