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RAZIA LATIF, MB; THOMAS C. SHOPE, MD

Am J Dis Child. 1983;137(8):801-802.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

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 . . . [Full Text PDF of this Article]

Author Affiliations
Wayne State University School of Medicine Detroit; University of Michigan Medical Center Ann Arbor

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