To clarify the cause of herpes zoster in immunocompetent children, specific humoral and cellular immunity was determined using an ELISA and a lymphoproliferative assay, respectively, in infants < 1 year of age and children > or = 1 year of age who had chickenpox. Thirteen (59.1%) of 22 infants, 17 (81.0%) of 21 children > or = 1 year of age (P < .02), and 13 (86.7%) of 15 children > or = 2 years of age (P < .001) had positive varicella-zoster virus (VZV)-specific cellular immunity. VZV-specific antibodies in infants were significantly lower than those in children > or = 1 year old (P < .01) and > or = 2 years old (P < .001). The possibility of subclinical reactivation was demonstrated by an increase in the specific cellular or humoral immunity (or both) in all of 6 infants who had negative specific cellular immunity. The low response of specific immunity and the immunologic evidence of reactivation in infants after chickenpox provide a possible explanation for the finding that chickenpox in infancy is a risk factor for herpes zoster.

No abstract

We examined specific humoral and cellular immunity from varicella-zoster virus (VZV) in 10 pediatricians, 8 healthy immune adults, 2 non-immune adults, and 15 patients with acute lymphocytic leukemia (ALL) in order to investigate the mechanism of resistance to VZV and the booster effect of frequent re-exposure. The responder cell frequency (RCF) against VZV antigen was determined by lymphoproliferative response with limiting dilution. Four of the 10 children with ALL and receiving maintenance therapy did not have VZV-specific cellular immunity according to our positive criteria (Stimulation Index > 2.0 and RCF > 1:150,000), but 3 of these 4 patients had VZV-specific IgG antibody. In both healthy adults and ALL patients re-exposure to VZV or reactivation of the virus enhanced VZV-specific immunity. Individuals with very high RCF values (> 1:10,000) had the lowest IgG antibody titers.

We determined natural killer cell (NKC) activity in 10 otherwise normal children with herpes zoster. NKC activity values in children with vs. without varicella-zoster virus specific IgM antibodies and in controls were 28.3 +/- 8.6%, 11.9 +/- 3.6% and 20.2 +/- 3.8% (mean +/- SD), respectively. There were significant differences between the children with and without IgM antibodies during the acute phase (p < 0.005) and between children without IgM antibodies and controls (p = 0.005). NKC values in children with mild vs. moderate morbidity were 11.7 +/- 4.1% and 25.7 +/- 9.9%, respectively (p < 0.05). The morbidity was moderate in all children with IgM antibodies, but in only 2 of the 5 children without IgM antibodies. Children who contracted varicella when a few months old had the highest IgM antibody titers and the highest value of NKC activity. NKC activity was related both to the presence of IgM antibodies and to the morbidity of herpes zoster.

We report on a 19 month old female who has been retarded developmentally after a severe varicella infection contracted from her mother 4 months after delivery. Her titer of varicella-zoster virus (VZV) IgG antibody has been remarkably high for 4 years after the infection. Natural killer activity and the specific cellular immunity to VZV, as tested by delayed type hypersensitivity skin test and lymphocyte-proliferation assay, were impaired. She had an improvement of ataxia and then progressed developmentally after administration of an anti-viral agent. Administration of oral corticosteroids and methylprednisolone transiently decreased titers of VZV antibody and, contrary to previous reports, returned natural killer activity to normal levels. We suggest that this case may be a persistent VZV infection similar to congenital cytomegalovirus infection due to selective defects in cellular immunity including NK cells. Whether this specific deficient cellular immunity is genetically determined or secondary to the viral infection is speculative. This is the first known report of such a case.