Studies on Respiratory Syncytial Virus Infection in the Ferret

摘要

The ontogency of the ferret humoral immune response was defined, and immunoglobulin and RSV antibody are transferred to the infants entirely in the products of lactation. If mother ferrets are infected with RSV antepartum, their offspring are protected against RSV replication both in the nose and lung. The protection is viral specific, effective only if infants are nursed by a previously infected mother prior to virus challenge, can be transferred for at least 8 days postpartum, and disappears after weaning. The degree of protection is correlated with the maternal neutralizing antibody titer or concomitant factor, but there is evidence that the antibody is not the sole means of protection. Maximal oral or parenteral doses of high-titered ferret RSV antiserum fail to protect infant ferrets from RSV challenge. Experiments with lung organ fragment and monolayer cultures indicate that the decreasing susceptibility of ferret lung to RSV replication with increasing age can also be observed in the cultures, strongly suggesting that intrinsic tissue maturation may be partially or wholly responsible for the age dependence of RSV replication in the ferret. When vesicular stomatitis virus was used as a specificity control for RSV experiments, it was observed that this agen could cause abortions and neonatal deaths in ferrets. A marked improvement in the glucose oxidase immunoenzyme technique was made, enabling us to show viral antigens, including RSV, in formalin fixed, paraffin embedded material from both the experimentally infected ferrets and from humans who were immunosuppressed.