Immunological Studies of herpes simplex virus infection in children with atopic eczema

Summary This study examines the role of immune defence mechanisms in herpes simplex virus (HSV) infections in atopic eczema and whether impairment of these mechanisms explains the susceptibility of some children with atopic eczema to cutaneous HSV infections. Ten children with eczema herpeticum and 13 with atopic eczema and recurrent HSV infection affecting multiple skin sites were studied, together with relevant control groups. In all children with atopic eczema, in vitro lymphoproliferation in response to stimulation with concanavalin A (Con A) was significantly decreased and natural killer (NK) cells (CD16 + 56) were reduced compared with non‐atopic controls. IL‐2 receptors, a marker for lymphocyte activation, were decreased during the acute phase of eczema herpeticum, and for 1 month thereafter. A positive stimulation index (>3) to HSV antigen, and high HSV lgG antibody titres measured by ELISA. Western blotting and neutralization assay, were seen in children with eczema herpeticum by 6 weeks, and also in children with atopic eczema and recurrent HSV infections. No evidence of an HSV‐specific immune defect (either cell‐mediated or humoral) was found in atopic eczema. Impairment of cell‐mediated immunity in atopic eczema and recurrent HSV infections. No evidence of an HSV‐specific immune defect (either cell‐mediated or humoral) was found in atopic eczema. Imairment of cell‐mediated immunity in atopic eczema was suggested by the reduced response to Con A. It is likely that reduced numbers of circulating NK cells and a decrease in IL‐2 receptors during early eczema herpeticum contribute to the susceptibility of children with atopic eczema to cutaneous HSV infections.