Abstract
Herpes zoster is caused by reactivation of varicella zoster virus (VZV) within the sensory ganglia and spread through the peripheral nerves into the skin of the corresponding dermatomes.
We studied the histological changes of the skin lesions in patients with herpes zoster and examined the distributions of VZV antigens using two monoclonal antibodies detecting either nucleocapsid or glycoproteins of VZV on paraffin sections of formalin fixed biopsy material. VZV infection within the skin begins at the follicular epithelia or lower epidermis at first, then spreads to the macrophages, fibroblasts, vascular endothelia of the small vessels, and perineurium of cutaneous nerves in the dermis.
Viral infections of the vascular endothelia around the involved follicles or vesiculated epidermis induce severe inflammation such as leukocytoclastic vasculitis and tissue destruction. In regard to the cutaneous nerves, VZV infections are observed within the perinerium, Schwann cells and vascular endothelia of neighboring vessels in the early erythematous or vesicular stages. In the full developed pustular or ulcerated stages, inflammatory cell infiltrates within the nerves and degeneration of the myelin sheath were observed. In the stage of postherpetic neuralgia, increase of thin nerve fibers without myelin sheath and intra fascicular fibrosis were observed.
