- Volume 21, Issue 1, 1973

When the chorioallantoic membrane of the embryonated hen’s egg was inoculated with herpes simplex virus type 2 strains, an infection resulted which spread rapidly throughout the egg. Haemorrhage and death occurred in the embryo, and haemorrhage was also observed in the chorioallantoic membrane. Virus was recovered from the infected chorioallantoic membrane, allantoic fluid, amniotic fluid and selected organs of the embryo. In contrast, similar inoculation of herpes simplex virus type 1 strains gave no haemorrhage in chorioallantoic membrane or embryos, embryos did not die and virus was recovered only from the inoculated chorioallantoic membrane. Inoculation of either type into the allantoic cavity did not result in spread of virus to the embryo. Prolonged adaptation of herpes simplex viruses to growth in eggs eventually resulted in spread of type 1 virus from the chorioallantoic membrane to other regions of the egg and there were also marginal increases in virulence of type 2 virus.

Prolonged passage of Marek’s disease virus in cell culture resulted in attenuation of the virus and inability of the virus to produce the membrane antigen. However, the apathogenic herpes virus of turkeys produced a serologically similar membrane antigen. Cell culture passage did not cause any change in production of intracellular antigens.

Evidence is presented that, in FV-3 infected BHK cell nuclei, the inhibition of RNA synthesis is paralleled by chromatin condensation. Inhibition of DNA synthesis could be due to the unavailability of the condensed chromatin to act as template.

Frog virus 3 inhibits the replication of various RNA viruses: nuclear and cytoplasmic, coated and uncoated, large and small. The inhibition is apparent at 37 °C, a non-permissive temperature for frog virus 3. Frog virus 3 particles must be present in the cell during the RNA replication in order to achieve inhibition. Our results indicate that the inhibition occurs in the early stages of virus replication.