Reactivation of latent VZV from human ganglia is a well-recognised complication of immunsuppression resulting in a variety of neurological complications, due, as indicated above, to symptomatic impairment of cell-mediated immunity to the virus. Indeed VZV infections are among the most important of all viral infections that affect the central nervous system (CNS) and peripheral nervous system (PNS) in immunocompromised individuals. The protean manifestations of VZV-induced neurological disease have been described in detail elsewhere [
6], but the main complications include herpes zoster (shingles) followed by post-herpetic neuralgia (PHN) in some cases the incidence of which rises with increasing age, VZV vasculopathy, myelitis, and
zoster sine herpete where VZV reactivates in the absence of the typical zosteriform rash [
16,
17,
18]. In chronic graft versus host disease following bone marrow transplantation VZV reactivation is also a recognised opportunistic viral infection that may mimic lymphoma [
19]. Treatment should be given to immunocompromised patients with herpes zoster consisting of intravenous acyclovir (in adults 10–15 mg/Kg 8 hrly for 10–14 days and in children 500 mg/m
2 for 7–10 days) (Class IV). The role of acylcovir in imunocompetent individuals below 50 years is less clear. In patients with VZV-induced myelitis and vasculopathy it has been suggested that treatment should be with intravenous acyclovir for 14 days in combination with oral prednisolone for 5–7 days but this is based on experience with only a small number of patients [
20] (Class IV). The diagnosis of an opportunistic VZV infection, including
zoster sine herpete can be obtained using PCR to detect VZV DNA in the CSF (Class III, Level C), though detection of anti-VZV IgG in the CSF has a higher sensitivity for correctly diagnosing VZV vasculitis than does PCR [
21]. The importance of host immunogenetics in determining VZV infection of the nervous system has recently been demonstrated. Thus it was shown that defects in the DNA sensor RNA polymerase III (POL III) confer selective increased susceptibility to infection of the central nervous system (CNS) causing encephalitis [
22,
23] and such hereditary immune defects may result in reduced production of Type 1 Interferon which reduces the host’s anti-viral capacity. The role of zoster vaccination for the immunocompromised patient is currently not established.