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

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