Louping ill virus proved to be pathogenic for young guinea-pigs, about 20 days old weighing about 150-180 g. In older guinea-pigs there was inapparent infection with virus replication in the brain and spleen, inflammatory lesions of encephalitis but without clinical signs or mortality. In non-immunosuppressed guinea-pigs virus replication was noted in the brain and spleen only during the first 5 to 7 days after infection. Serum antibodies appeared on the 3rd day, increased quickly and reached the maximum after 9 days, remaining at the same level for up to the 51st day. In immunosuppressed animals replication of virus in the brain was similar during the first 7 days to that of untreated guinea-pigs, but thereafter, it increased considerably reaching 105 LD50 of virus by the 15th day and later, although in diminished quantities, persisted for at least 29 days after infection. Replication of virus was not demonstrated in the spleen of immunosuppressed animals during the first 7 days, but virus appeared on the 9th day, attained a peak by the 15th day; after a slow decline it could still be detected by the 25th day. Serum neutralizing antibodies after a very short appearance between the 3rd and 5th day, declined quickly and disappeared almost completely until the 12th day. From the 15th day the amount of antibody increased reaching the top level by the 22nd day, and remained so at least until the 51st day after infection.
Inflammatory and degenerative brain lesions were noted in both immunosuppressed and non-immunosuppressed animals, but whereas the curve representing inflammatory lesions followed the pattern of serum antibodies, the degenerative changes appeared to follow the pattern of virus replication. While inflammatory changes were present in non-immunosuppressed animals beginning from the 3rd day, in immunosuppressed guinea-pigs no inflammatory lesions were detected until about 12-15 days after infection. The absence of inflammatory lesions at the beginning of infection in immunosuppressed animals, coincided with the critical decline in the presence of serum antibodies. Although lesions were present in most parts of the brain the most severe and constant lesions were found invariably in the cerebellum.
The successful tracing of louping ill virus by immunofluorescence proved that this method is highly sensitive and that it could be adapted for reasonably accurate quantitation of virus.