A primitive immunoligic marker of intrauterine virus infection

Abstract

Retrospective and prospective studies of the human have suggested that intrauterine mumps virus infection evokes an incomplete immunologic response of delayed hypersensitivity, without humoral antibody. Experimental infection of the subhuman primate during the first third of pregnancy also leads to the development of only cellular immunity in the infant offspring. The significance of delayed hypersensitivity as an immunologic marker of fetal infection is strengthened by the observation of an anamnestic neutralizing antibody response in 2 of 4 infant monkeys following a second skin test. Repeated skin testing of 5 seronegative adult monkeys failed to induce a primary antibody response. Intrauterine mumps virus infection illustrates the phylogenic and ontogenic concept that cellular immunity is the most primitive immunologic response. Experimental infection of 9 monkeys between the 25th–40th day of gestation, with subsequent cesarean section after 1, 2 and 3 weeks, has demonstrated that virus multiplies in the young fetus for only 1 week. Fetal interferon response does not occur, so the termination of viral replication seems to result from transplacental distribution of abundant 7S maternal neutralizing antibody. This conclusion is supported by the restrictive effect of antibody on mumps virus replication in vitro. Thus, the immature fetus confronts minimal antigenic mass and accrues immunopoietic instruction for only the more primitive response of delayed hypersensitivity.