Aleutian disease virus, the causative agent of a persistent infection in mink, was isolated in a continuous line of feline renal cells when the cultures were maintained at reduced temperature (31.8°). After serial in vitro passage of the virus at this temperature it had an optimum replication temperature of 37°. An immunofluorescence focus assay was found to be suitable for virus quantitation. The cultured virus reproduced Aleutian disease in mink, and the virus could be reisolated from the mink 10–180 days after inoculation. The properties of the virus suggest that it is a member of the parvovirus group.

Herpesviruses isolated from either domesticated or wild carnivores should be immunologically compared with known viruses of this group which could have been included in the diet of the animal before being considered to be previously undescribed herpesviruses native to the carnivore in question.

Although scrapie is clearly a transmissible disease caused by a small stable agent, previous conventional attempts to demonstrate humoral antibody have not met with success. In this study no evidence of humoral antibody to the scrapie agent was found in infected mice by regular or antiglobulin potentiated neutralization tests, indirect immunofluorescence tests employing various agent-containing targets, or by examining brains, spleens, and kidneys for the presence of immune complexes. The results suggest that scrapie infection is fundamentally different from slow or persistent virus infections in which humoral antibody may be demonstrated by the techniques used in this study.

Aging mice frequently develop a glomerulosclerosis; the severity of the lesion varies among mouse strains and increases with age. The kidneys of fifty 1-year-old C57BL/6 mice were examined and 48 had histologic evidence of mild to moderate intercapillary glomerulosclerosis. All fifty mice had glomerular deposits of IgG and 41 had deposits of C3 which were located in the mesangial zone and along glomerular capillary walls. Fifty to 57% of the kidney-bound immunoglobulin which was eluted reacted with murine leukemia virus cell surface antigen, while 8 to 37% of the immunoglobulin reacted with syngeneic erythrocytes. The glomerulosclerosis of aging C57BL/6 mice appears to be an immune complex glomerulonephritis induced by murine leukemia virus antigens, and to a lesser extent, erythrocyte antigens.