Rhesus monkey fetuses of either immune or nonimmune dams were inoculated in utero with Adenovirus SV-20 (AdSV-20), a virus capable of inducing fetal pneumonia, and studied immunologically at various intervals. AdSV-20 infection at 90-100 days gestational age resulted in absolute lymphopenia in a few fetuses, reduced numbers of peripheral blood lymphocytes (PBL) which formed rosettes with sheep erythrocytes (ERL) and reduced complement-receptor lymphocytes (CRL) in a majority, while Fc fragment-receptor lymphocytes (FcRL) were occasionally increased. There was a tendency for depression of ERL and CRL early in infection of 120-130-day fetuses, followed by stimulation of these populations and FcRL in later phases. Maternal immunity did not protect against these effects of AdSV-20 infection in fetuses. Immune and nonimmune dams were spared adverse clinical effects and had no changes in lymphoid cell populations following inoculation of their fetuses. Despite precocious production of circulating IgM, fetuses of nonimmune dams had little or no demonstrable anti-AdSV-20 serum neutralizing (SN) antibody, indicating that the ability to develop an effective immune response was suppressed or had not been acquired at the gestational ages studied. Nonimmune dams displayed little evidence of seroconversion following inoculation of their fetuses with AdSV-20, except in those dams whose fetuses died in utero, whereby there was a significant antibody response. SN antibody titers of immune dams were not boostered substantially subsequent to inoculation of their fetuses, and fetal SN titers were lower than maternal titers, suggesting absence of an active fetal antibody response in this group also. Direct inoculation of AdSV-20 into 90-130-day rhesus monkey fetuses provided a model system for immunologic study of fetal infection, probably involving complex fetal-maternal interactions, in a situation where the infected, viable fetus and its dam appeared to be microbiologically isolated from one another.
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