## Varicella-Zoster Virus (VZV) — Latency and Reactivation **Key Point:** VZV establishes latency in sensory ganglia (dorsal root, trigeminal, geniculate) and reactivates to cause herpes zoster (shingles) in a dermatomal distribution. **High-Yield:** Herpes zoster occurs in ~30% of the population during their lifetime; incidence increases dramatically with age (>50 years) and immunosuppression (HIV, malignancy, post-transplant). ### VZV Reactivation Triggers - Aging and waning cell-mediated immunity - Immunosuppression (HIV/AIDS, chemotherapy, biologics) - Physical trauma or stress - Sunlight exposure (especially in ophthalmic distribution) - Concurrent malignancy **Clinical Pearl:** Prodromal pain or paresthesia precedes the rash by 2–3 days. Post-herpetic neuralgia (PHN) is the most common complication in elderly patients, persisting months to years after rash resolution. **Mnemonic:** **DERM** — Dorsal root ganglia, Eruption in dermatomal pattern, Reactivation triggered by stress/age, Mononuclear infiltrate on histology. ### Distinguishing VZV from HSV | Feature | VZV | HSV | |---------|-----|-----| | Latency site | Dorsal root ganglia (sensory) | Sensory ganglia (trigeminal, sacral) | | Distribution | Dermatomal (unilateral) | Non-dermatomal (often bilateral or recurrent at same site) | | Recurrence rate | Lower (~30% lifetime) | Higher (frequent recurrences) | | Age of reactivation | Typically >50 years | Any age | | Prodrome | Dermatomal pain 2–3 days | Localized tingling, burning |
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