Biomedical subjects
Publications and source records attributed to R F Marsh.
Brain preparations from animals with scrapie or transmissible mink encephalopathy were phenol extracted and examined for the presence of pathogenic nucleic acid. Animals inoculated with various extracts remained healthy, and analysis on 2.6 to 5% polyacrylamide gels failed to detect a difference in extractable RNA species between infected and normal mink brain.
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Eighty-three percent of hamsters inoculated at birth with JC virus, a human papovavirus isolated from brain tissue of a case of progressive multifocal leukoencephalopathy, developed malignant gliomas within 6 months. Three brain tumors have been serially transplanted as subcutaneous tumors. JC virus was isolated from five of seven tumors tested. Cells from four tumors were cultivated in vitro. These cells contained an intranuclear antigen with the characteristics of a T antigen, and this antigen was antigenically related to SV40 T antigen. Although virus was not recovered from extracts of serially cultured tumor cells, JC virus was rescued when one tumor cell line was fused with permissive cells.
Circulating lymphocytes from mink with transmissible mink encephalopathy were studied for the presence of virus particles and for infectivity. Electron microscope examination of phytohemagglutinin-stimulated lymphocyte cultures revealed no evidence of virus-like particles. Circulating lymphocytes were also found to be noninfectious when the transmissible agent could be demonstrated in intact lymphoid organs in infected mink. A lymphopenia was detected in affected mink during the late clinical stage of disease, but this was most likely a secondary effect due to a terminal stress factor.
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A progressive, fatal spongiform polioencephalopathy was induced in mink intracerebrally inoculated with a suspension of brain from a Suffolk sheep with naturally acquired scrapie. The clinical signs and pathological lesions of the experimental disease were indistinguishable from transmissible mink encephalopathy, a disease of undetermined origin that occurs in mink.
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A progressive, fatal spongiform encephalopathy developed in three squirrel monkeys 11 months after inoculation with primate-passaged transmissible mink encephalopathy agent. The clinical symptoms and histopathologic and electron microscopic findings suggest that this naturally occurring disease of mink has been transmitted experimentally to squirrel monkeys.
Attempts to demonstrate specific serum antibody or immune complexes in the brains of mink affected with transmissible mink encephalopathy were unsuccessful with serum neutralization and immunofluorescent procedures. These data may be significant, considering the unusual nature of the disease and the biochemical properties of the etiological agent.
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The size of the transmissible mink encephalopathy (TME) agent is estimated to be less than 50 nm on the basis of its passage through membrane filters. The agent is sensitive to ether, relatively resistant to 10% Formalin, resistant to ultraviolet irradiation, and susceptible to proteolytic digestion with Pronase. Attempts to extract an infectious nucleic acid fraction with hot phenol were unsuccessful. The results of these studies indicate that the TME agent has biochemical properties which are similar to those described for the transmissible agent of scrapie.
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Transmissible mink encephalopathy (TME) is probably a form of the sheep disease, scrapie, introduced by accidentally feeding mink with scrapie-infected sheep tissues. Although no successful transmissions of TME to mice have been achieved previous work has involved various limitations. To maximize the possibility of transmission, 176 mice, representing 14 different genotypes mostly not previously tested with TME, were injected with TME-infected mink brain from three sources with different histories. No scrapie-like disease was detected clinically or histologically in these mice or in a further 111 which were subsequently injected with brain or spleen material from 10 of the TME-injected mice killed when senile. Furthermore, a series of experiments involving seven strains of scrapie, demonstrated that prior injection of mice with TME failed to affect the normal progress of scrapie infection indicating that TME agent had not occupied scrapie replication sites or otherwise influenced the pathogenesis of scrapie. The overall conclusion from these experiments is that TME is biologically inactive in mice. Although many strains of natural scrapie can be transmitted to laboratory mice, this has not been possible with all strains and it is concluded that one or more of such strains is likely to be the cause of TME in mink.