Aetiology
HZ results from reactivation of latent varicella-zoster virus (VZV) from dorsal root or cranial nerve ganglia, present since primary infection. VZV is a double-stranded DNA herpes virus, spreading from direct person-to-person contact with an infected individual or lesion and from air droplets. Latent infection, after primary infection, is established by evading the immune system through the reduction of the number of genes expressed and downregulation of the expression of major histocompatibility complex class I antigens on the surface of the infected cells.[22] HZ and 'chicken pox' or varicella are both caused by the same virus, but varicella usually follows the initial infection and causes a generalised rash, whereas HZ occurs after reactivation of a previous infection and tends to be localised to a specific nerve distribution.
Pathophysiology
After a primary varicella-zoster virus (VZV) infection, the virus establishes latency in dorsal root and cranial nerve ganglia. In immunocompetent people, the infection usually affects a single dermatome, with rare involvement of multiple dermatomes. However, in immunocompromised people, the involvement of several dermatomes is common. A decline in the virus-specific cell-mediated immunity as a result of HIV, malignancies, chemotherapy, or chronic use of corticosteroids results in the reactivation of infection, which spreads from the ganglion to the neural tissue of the affected segment and the corresponding cutaneous dermatome.[1] The reactivation leads to ganglionitis: inflammation and destruction of neurons and supporting cells. The virus is also carried down the axons to the areas of the skin innervated by the affected ganglion, causing local inflammation.
Characterised by a prodromal period with burning pain for 2 to 3 days, a vesicular eruption follows in the dermatomal distribution of the infected ganglion. Any dermatome may be affected; however, the most commonly affected dermatomes are T1 to L2.[22] Although sensory neurons are most commonly affected, in 5% to 15% of patients motor neurons are affected as well.[3]
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