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Herpes zoster (shingles) is caused by reactivation of latent varicella-zoster virus (VZV) in the dorsal root ganglia or cranial nerve ganglia, years to decades after primary infection (chickenpox). It presents as a painful, unilateral, dermatomal vesicular eruption.

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Shingles (Herpes Zoster): Pathophysiology, Risk Factors, Phases of Infection, Symptoms, Treatment

https://www.youtube.com/playlist?list=PLkdHelTlDZnG9VE2lDUVNfDYibvMEN5qg

Epidemiology

• Lifetime risk: ~20–30% (higher with increasing age)
• Peak incidence: >50 years
• Increased risk in immunocompromised patients (HIV, malignancy, transplant, steroids)

Pathophysiology

• After primary varicella infection, VZV remains latent in sensory ganglia
• Reactivation → viral replication → neuritis and radiculitis
• Virus spreads centrifugally along sensory nerves to the skin, producing dermatomal rash
• Neuronal damage underlies acute pain and postherpetic neuralgia

![Natural history of herpes zoster: primary varicella infection induces immunity via development of antigens (not shown) and varicella-zoster virus (VZV)-specific memory T cells. T cell–mediated immunity declines with age until, below threshold point (dashed line) risk for zoster reactivation increases. Exposure to zoster, whether as VZV reactivation or vaccination, boosts immunity and protects against subsequent episodes.

Data from Arvin A. N Engl J Med 2005;352:2266-7. Weinberg JM. Herpes zoster: Epidemiology, natural history, and common complications. Journal of the American Academy of Dermatology. 2007;57(6):S130-S135. doi:https://doi.org/10.1016/j.jaad.2007.08.046](attachment:d36894d7-0d12-44eb-b2a1-f23bb6dade74:1-s2.0-S0190962207014429-gr1_lrg.jpg)

Natural history of herpes zoster: primary varicella infection induces immunity via development of antigens (not shown) and varicella-zoster virus (VZV)-specific memory T cells. T cell–mediated immunity declines with age until, below threshold point (dashed line) risk for zoster reactivation increases. Exposure to zoster, whether as VZV reactivation or vaccination, boosts immunity and protects against subsequent episodes.

Data from Arvin A. N Engl J Med 2005;352:2266-7. Weinberg JM. Herpes zoster: Epidemiology, natural history, and common complications. Journal of the American Academy of Dermatology. 2007;57(6):S130-S135. doi:https://doi.org/10.1016/j.jaad.2007.08.046

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Commonly Affected Dermatomes

• Thoracic (most common)
• Cranial nerves – especially trigeminal (V1 > V2 > V3)
• Cervical and lumbar dermatomes