Herpes Zoster: A Clinical Review

St. Mary’s Hospital, Division of Infectious Diseases, Waterbury, Connecticut, USA. Received for publication: August 13, 2011. Reprint request: Birinder S. Singh, M.D., St. Mary’s Hospital, Division of Infectious Diseases, Waterbury, Connecticut, USA. INTRODUCTION Varicella zoster virus (VZV) is a ubiquitous human virus that belongs to the subfamily alphaherpesvirinae.1 It contains the smallest genome of the herpesviruses. It is an icosahedral shaped, enveloped virus that measures approximately 200 nanometers in diameter. The virus has more than 30 structural proteins as well as glycoproteins.2 Varicella zoster causes two distinct syndromes. The initial infection first presents as varicella or ‘chickenpox’, which is a contagious and usually self -limiting illness. It occurs in epidemics amongst susceptible children.3 On resolution of the primary infection, the virus migrates from sensory nerve endings to reside in the dorsal root ganglion.4 When cell mediated immunity declines (Table 1) below a crucial level, reactivation of this virus results in herpes zoster (HZ) or ‘shingles.’ The words “herpes zoster” are derived from the Greek herpein, meaning “to spread or creep” and zoster, meaning “girdle or zone.” ‘Shingles’, another word of Greek origin, means “girdle”, a reference to the dermatomal distribution characteristic of this disease.2 This migration and eventual colonization along this neural route explains the distribution of rash along a sensory nerve dermatome.4 In utero infection leading to childhood zoster is another possible, albeit rare, mechanism for acquiring herpes zoster. This has been reported in children as young as four months.4