Abstract
Summary
Previous studies have revealed that SMCA-infected mice confer protection against the effects of SMCA or GT-48 virus infection on their progeny, despite the fact that tests using an in ovo assay system consistently revealed very low antibody titers in the sera of infected mice. In the present studies, protective activity in the serum of infected mice was demonstrated by its ability to confer passive protection on GT-48 virus-inoculated suckling mice. Mouse or rabbit origin antisera were also demonstrated to confer passive protection on SMCA or GT-48 virus-inoculated suckling mice when inoculated into the dam at the time of challenge of the progeny. The neutralizing antibody in antisera prepared in mice and rabbits was assayed by means of a neutralization index test using GT-48 virus and assay of serum-virus mixtures in i.c. inoculated suckling mice. This test proved to be reliable and sensitive. When serum was diluted, neutralizing capacity decreased disproportionately, even when such accessory factors as fresh mouse serum or guinea pig complement were added. Virus-antibody dissociation was demonstrated following dilution of a reaction mixture of SMCA mouse antiserum and GT-48 virus. Approximately 1% of apparently previously neutralized virus activity was recovered immediately upon dilution of the serum-virus mixture at 4°. The antibody response in SMCA-inoculated newborn mice was studied. Normal mice inoculated with SMCA as newborns have been shown to acquire a lifelong ability to protect their progeny against SMCA. Such mice had no detectable circulating antibody at 5 days of age, but developed high titers (NI > 5.0) of antibody by 20 days, which then persisted until at least 240 days of age. Newborn mice inoculated with SMCA under the influence of maternal immune protection cannot subsequently confer protection on their own progeny. These mice had high-titered circulating antibody at 5 days of age that diminished to a persisting low level (NI = 2.0) by 40 of age.
Get full access to this article
View all access options for this article.
