With pseudorabies virus, section of the sciatic nerve with inoculation into the ipsilateral foot pad significantly retarded the speed of infection. The virus ascended other nerves of the leg, but at a slower rate. It would appear that the number of nerve fibers available for passage may play a rôle in the speed with which infection occurs with this virus.

When pseudorabies virus was inoculated into an area of inflammation its effects were markedly lessened. Similar experiments with unmodified equine encephalomyelitis virus which, unlike pseudorabies, does not ascend along local nerves, showed no impedance of infection.

Brain trauma did not change the rate of infection with the viruses of St. Louis encephalitis, herpes, or pseudorabies. But intraperitoneal injection of glycerine, followed by intramuscular inoculation of St. Louis virus, resulted in marked facilitation of infection, as already remarked of fixed equine encephalomyelitis virus. This phenomenon did not occur with pseudorabies or herpes.

In contrast to certain other viruses, pseudorabies and herpes viruses were only slightly more effective in young mice than in adults.

With St. Louis virus, as with fixed equine encephalomyelitis viruses, inoculation into the eye or nose was far more effective than other peripheral routes. This was not the case with pseudorabies. Herpes, however, also showed greater sensitivity of the intraocular route.

After injection into the eye, St. Louis and fixed equine encephalomyelitis viruses invaded the optic pathway, while herpes and pseudorabies avoided the optic fibers and attacked the trigeminal nerve. These phenomena are discussed in the light of cellufugal and cellupetal progression of viruses.

The similarities in the action of fixed equine encephalomyelitis and St. Louis encephalitis viruses are discussed and contrasted with herpes and pseudorabies.