Abstract
Measles is characterized by lifelong immunity and a transient immunosuppression which, in developing countries, is responsible for a high morbidity and a high mortality consecutive to secondary infections. Strickingly, the immune suppression is coincident with MV-specific immunity and continues for several weeks after apparent recovery from measles. The immune suppression is characterized by the loss of delayed-type hypersensitivity skin test responses to recall antigens, such as tuberculin, and by the inhibition of antibody production and cellular immune responses to new antigens (1).
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