Varicella zoster virus tissue tropism – a target in vaccine development

Varicella-zoster virus (VZV) is a ubiquitous, neurotropic human herpesvirus and the causative agent of both varicella (chicken pox) and herpes zoster (shingles) [1]. Varicella is a highly infectious disease caused by primary infection of VZV and characterized by itchy, red pockmarks covering the entire body [2]. Although varicella is considered a benign and self-limiting childhood illness, it can cause severe disease in both immunocompetent and immunocompromised individuals [3].

During varicella, the virus infects the sensory neurons and establishes lifelong latency. In an immunocompromised state, or a state of immunosenescence, the latent virus can reactivate and manifest as a painful belt-like rash, which is termed herpes zoster [4]. Replication and spread of the virus within the ganglion can cause neuronal necrosis and inflammation, which may in turn be linked to post-herpetic neuralgia (PHN) [5, 6]. PHN is a chronic neuropathic pain that might last from months to years owing to the resulting nerve damage [7, 8]. The incidence and severity of both zoster and PHN increases with age [9], greatly compromizing quality of life in the elderly and presenting a burden for the aging society.

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