Mechanism of the Teratogenic Action of Newcastle Disease Virus in the Chick Embryo

Open Access
Publisher Website
Google Scholar
Abstract
Summary: Evidence has been presented indicating that defects in early chick embryos, after inoculation of allantoic fluid suspensions of Newcastle disease virus, resulted from the presence of the fully infective virus and probably were due to the proliferation of the virus since, in all circumstances observed, they were associated with this phenomena. Homologous immune globulin prevented the teratogenic action of the virus suspensions, and no teratogenic activity was found in suspensions from which the virus particles had been removed by ultracentrifugation. Virus inocula, inactivated by heat or ultraviolet irradiation, failed to produce defects. Inoculation of inactivated virus decreased somewhat the yield of abnormal embryos following subsequent inoculation of active virus. There was no conclusive evidence that the rate of multiplication in organs, showing characteristic defects, was greater than that of tissues which appeared unaffected. It seemed clear, however, that virus proliferated in other tissues as well as those showing gross defects. Microscopic studies showed that dilute virus inocula produced characteristic cell damage of a relatively mild type in comparison to the gross defects following concentrated virus inocula, but that the organ specificity was the same in either case.