Elderly subjects (age 75-95 years) immune to varicella zoster virus (VZV) were identified by the presence of serum IgG antibody. The frequency of lymphocytes in their blood which proliferated in varicella zoster virus antigen-stimulated cultures was 1:78,000 +/- 6600. This is less than the 1:14,000 +/- 2000 frequency of VZV-responsive lymphocytes in blood from younger adult (20-43 years) donors. Elderly donors' blood mononuclear cells were less efficient than those of younger adults at lysing VZV-infected fibroblasts but not K562 target cells. The lysis of VZV target cells by elderly donors' MNC increased to control levels in the presence of 10 U/ml of interleukin-2 (IL-2). These results suggest that mononuclear cells capable of killing VZV-infected target cells persist with aging but that reduced numbers of antigen-responsive and lymphokine-releasing T cells may limit their function.

Epstein-Barr virus-transformed human B cells expressed cell surface varicella-zoster virus (VZV) antigens after superinfection with VZV although they did not form infectious centers in a plaque assay. The VZVsuperinfected cells were lysed by autologous VZV-stimulated T-cell lines and their derivative clones. The effector cells were specific for VZV and an HLA DR antigen and were T4+. The specificity of lysis of Epstein-Barr virus-transformed, VZV-superinfected targets by prestimulated mononuclear cells in this system contrasted with the unrestricted lysis seen when the targets were VZV-infected fibroblasts.

Human newborns are susceptible to severe infections with HSV (1) and those who recover have low frequencies of HSV specific responder T cells in their blood (2). The frequency of HSV-responder T cells in normal newborns is low (less than 1:106) (3) and host defense is thought to depend primarily on antibody passively acquired from the mother and on nonspecific effector mechanisms including the production of interferons and NK cells (4). Leukocyte (or a ) interferon is made in equivalent amounts by human newborn and adult blood MNC stimulated by HSV (5). Less is known of y-interferon, which is made by T cells (6, 7) and NK cells (8). This lymphokine has a wide range of biologic activities (9) including suppression of cell growth and herpes virus replication and the amplification of NK lysis of virus-infected target cells. Previous studies indicate that newborn blood MNC have a low frequency of T cells which make yinterferon spontaneously (10) and that they release less ?-interferon in response to phytohemogglutinin (1 1, 12), Concanavalin A, or OKT 3 antibody (Ortho Diagnostic Systems, Raritan, NJ) (12) than adult MNC unless the newborn MNC are first irradiated (12) or, in Taylor & Bryson's study (1 I), the newborn monocytes were replaced by adult monocytes. Phytohemogglutinin and Concanavalin A activate a wide range of cells so the existing data give no indication of the relative ability of newborn and adult NK cells to respond to a herpes virus stimulus. We

Ten survivors of neonatal HSV encephalitis had IgG1 and IgG3 antibodies to HSV 6 or more months after their infection. Six had IgG4 antibodies but only one had IgG2 antibodies. Titers of anti-HSV antibodies were similar following neonatal and later HSV infections. Antibody deficiency is thus not part of the selective deficiency of HSV-specific immunity following neonatal infection.

Blood T-cells from 28 patients with type I (insulin-dependent) diabetes (IDDM) of variable duration were examined for the Tac antigen by immunofluorescence, and for proliferation in the presence of interleukin 2 (IL 2). The mean percentage of Tac+ cells in patients whose IDDM was of less than 2-yr duration was 6.2% compared with 2% in patients whose IDDM was of 3 or more years' duration, or in healthy controls. The percentage of Tac+ cells in the patients' blood correlated positively with the amount of thymidine uptake in a 24-h culture of blood mononuclear cells and with the percentage of T-cell blasts generated in a 6-day culture. The patients' T-cell blasts stained with OKT 4 or OKT 8, suggesting that each of these subsets is present in the activated T-cell population in the patients' blood. The T-cell blasts did not show specificity for pork insulin in an antigen restimulation assay. There was no correlation between increased Tac+ cells and the presence or absence of islet cell antibodies. If T-cell activation in IDDM occurs as a result of recognition of islet cell antigens, our results suggest that both HLA-DR-restricted (OKT 4+) and A-, B-, and C-restricted (OKT 8+) T-cell subsets contribute.