Fig. 3.
A model of the pathogenesis of primary and recurrent VZV infection. VZV infection is acquired by inoculation of mucosal epithelial cells via the respiratory route, transfer across epithelial layers allows infection of T cells in tonsils and other lymphoid tissue that comprise Waldeyer’s ring and allows transport to the skin via a T cell-associated viremia. Infection of skin produces the vesicular rash characteristic of varicella. VZV may reach sensory ganglia by T cell viremia or during skin infection, VZ virions may gain access to the sensory nerve cell body by retrograde axonal transport; lifelong latent infection is established in sensory ganglia in the course of primary VZV infection. Clinical reactivation of latent VZV results in herpes zoster, during which VZ particles gain access to skin via anterograde axonal transport. Adapted from Zerboni and Arvin 2008