Disease Animation

Varicella-zoster virus establishes latency in cells of the dorsal root ganglia after primary infection.6 Zoster is caused by the reactivation of a virus that was dormant in sensory nerves from an earlier infection of
primary varicella.15

  • Varicella-zoster virus is a ubiquitous human alphaherpesvirus, which causes varicella (chickenpox) and zoster (shingles).
  • Zoster is caused by the reactivation of virus that was dormant in sensory nerves from an earlier infection of primary varicella.
  • The most distinctive feature of herpes zoster is the localization of the rash, which is unilateral, does not cross the midline and is generally limited to the area of skin innervated by one or adjacent dermatomes.

Latency:

Varicella-zoster virus is a ubiquitous human alphaherpesvirus, which causes varicella (chickenpox) and zoster (shingles). Varicella results from primary VZV infection; which is a common childhood illness associated with a generalized vesicular rash. VZV establishes latency in cells of the dorsal root ganglia during primary infection. VZV may reach dorsal root ganglia from the skin lesions by traveling along neuronal cell axons (depicted here) or it may be carried to these sites by infected peripheral blood mononuclear cells (PBMC).6

Reactivation:

Zoster is caused by the reactivation of virus that was dormant in sensory nerves from an earlier infection of primary varicella. Cellular immunity usually prevents the reactivation of varicella-zoster virus; however, waning of cellular immunity to the virus for example, with advancing age, is associated with clinical reactivation. Upon reactivation, infectious virus appears in neurons and nerve-associated satellite cells and spreads to the skin through peripheral nerves.15

The most distinctive feature of herpes zoster is the localization of the rash, which is unilateral, does not cross the midline and is generally limited to the area of skin innervated by one or adjacent dermatomes. The lesions of HZ consist of closely grouped vesicles in contrast to the discrete, randomly distributed vesicles of varicella. The localized appearance of the zoster rash is due to intraneural spread of virus to the skin, as opposed to viremic spread in varicella; clusters of vesicles occur where sensory nerve endings introduce VZV into the skin.7

In acute zoster, the skin may be inflamed and partially denervated, and the dorsal root ganglion may show inflammation, hemorrhagic necrosis, and neuronal loss. There may be scarring of the skin, peripheral nerves, and dorsal root ganglia. This damage to the nerve endings, nerve bodies and architecture of the dorsal root ganglia is thought to contribute to the persistent pain after rash healing.15

Information on Herpes Zoster Rates