Techniques for assay of in vitro lymphocyte transformation (LTF) were used with varicella-zoster virus (VZV) as the antigen to study the temporal characteristics of the VZV-specific cellular immune response in children with varicella and in normal subjects with a history of the illness. The LTF response in children with only vesicular eruptions was prompt, and individual peak activity was detected within one to two weeks after the onset of illness, followed by a gradual decrease of the activity to lower levels. Patients with a complication of meningoencephalitis showed a marked delay in the development of peak activity. No consistent defference in the development of complement-fixing antibody to VZV was observed in these patients with different clinical manifestations. The LTF response of normal subjects with remote clinical evidence of varicella was characterized by occasional high activity, a finding that suggests reinfection with VZV. These observations provide additional evidence that the specific cellular immune response is heavily involved in the pathogenesis of VZV infection.

A 9‐year‐old girl with leukemic infiltration of cells characterized by indented nuclei and abundant faintly acidophilic cytoplasm was autopsied. Electron microscopic studies of the cervical lymph nodes and tumor nodules in the liver and kidney (fixed in formalin solution for 3 years) together with the specimens taken from the cutaneous eruptions at autopsy demonstrated that the proliferating cells frequently contained Langerhans' granules in the cytoplasm. Accordingly, this case was thought to be a disease with systemic, progressive, and malignant proliferation of Langerhans' granule‐containing histiocytes (LGH). The intimate relationship between Letterer‐Siwe's disease and LGH has recently been recognized. Inasmuch as the present case satisfied both the clinicopathologic criteria of Letterer‐Siwe's disease and malignant histiocytosis, the proliferating histiocytes in both of them could be the same type of cell (LGH).

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An attempt to isolate cytomegalovirus (CMV) from specimens obtained from children with various diseases was carried out from June, 1966 thru August, 1967. Forty-five strains of CMV were isolated from 21 cases of 135 children examined. Success in isolation was most frequently observed in children ranging in age from 5 months to 4 years. Serological investigations revealed a rate of incidence of complement-fixing antibodies against CMV was over 90% in the newborn, decreased to 60% in infancy, and gradually increased after 10 years of age. The highest rate of primary infection incidence was in early infancy and it was noted that lower age infants showed a marked tendency to become persistent virus cxcreters.

Antibodies to human cytomegalovirus (CMV)-specific antigens were determined in sera serially collected from 10 infants with primary CMV infection. Antibodies to pre-early nuclear antigens (PENA), which are detectable in human embryonic lung cells within 3 h of CMV infection by anticomplement immunofluorescence staining, developed in all the patients. However, in contrast to the early response of anti-early antigens (EA), anti-late antigens (LA), and immunoglobulin M antimembrane antigens (MA), seroconversion or the maximum antibody response to PENA was usually observed 1 or more months later. Immunoglobulin M antibody to MA became undetectable soon after recovery from illness, followed by a decrease in anti-EA, anti-PENA, and then anti-LA titers. Results indicated analogy of the clinical significance of anti-PENA in CMV infection to that of anti-Epstein-Barr nuclear antigen in infectious mononucleosis and support the idea that parallel determinations of anti-PENA and IgM anti-MA antibodies can be useful for identifying the acute or chronic phase of primary CMV infection.