Primary infection with varicellazoster virus (VZV) causes chickenpox. After the primary infection, the virus remains dormant in the sensory ganglionic neurons until reactivated.1 The mechanism of reactivation is poorly understood, but various insults like malignant neoplasms, irradiation, immunosuppressive therapy, or aging cause reactivation of the virus, producing lesions of herpes zoster (shingles).2 While the incidence of chickenpox is greatest among the 5- to 9-year-old age group,3 the incidence of zoster, which may occur at any age after primary varicella infection, increases sharply after the age of 50 years.4 Herpes zoster in otherwise normal children occurs without any obvious predisposing cause. Extensive data are available regarding herpes zoster in adults2 and immunocompromised children,5-7 but little is known about this disease in immunologically competent children.8-10 We have compared the epidemiologic and clinical features of herpes zoster occurring in seven otherwise normal children with the same
LATIF R, SHOPE TC. Herpes Zoster in Normal and Immunocompromised Children. Am J Dis Child. 1983;137(8):801–802. doi:https://doi.org/10.1001/archpedi.1983.02140340081021
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