Varicella-zoster virus (VZV) establishes latency in dorsal root ganglia after primary chickenpox. During reactivation (herpes zoster), what is the mechanism of pain (post-herpetic neuralgia) that persists after skin lesion resolution?
- A Inflammatory demyelination and permanent destruction of dorsal horn inhibitory interneurons (central sensitization) ✓
- B Continued viral replication in peripheral nerves
- C Re-infection with HSV-1 at the same dermatome
- D Vitamin B12 deficiency triggered by viral infection
Correct answer: A. Inflammatory demyelination and permanent destruction of dorsal horn inhibitory interneurons (central sensitization)
Explanation
Post-herpetic neuralgia (PHN) results from damage to peripheral nociceptive fibers and permanent injury to inhibitory interneurons in the dorsal horn (spinal cord), leading to central sensitization. Loss of large myelinated inhibitory fibers disinhibits C-fiber pain transmission ('gate control' failure). Inflammatory cytokines during active zoster cause demyelination and axonal degeneration. Antiviral therapy (acyclovir/valacyclovir) initiated within 72 hours reduces viral replication and severity of PHN but does not eliminate it once established.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
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