Aleutian Disease of Mink

1980 ◽  
pp. 261-286 ◽  
Author(s):  
David D. Porter ◽  
Austin E. Larsen ◽  
Helen G. Porter
Keyword(s):  
Aleutian Disease Of Mink

Aleutian disease of mink

1963 ◽  
Vol 6 (4) ◽  
pp. 386-388 ◽  
Author(s):  
Bernard M. Wagner
Keyword(s):  
Aleutian Disease Of Mink

The Structure of the Aleutian Disease Antigen

1976 ◽  
Vol 34 ◽  
pp. 302-303
Author(s):  
N.H. Sarkar ◽  
G.W. Notani ◽  
A.J. Kenyon
Keyword(s):  
Disease Virus ◽  
Average Diameter ◽  
Icosahedral Symmetry ◽  
Structural Components ◽  
Virus Structure ◽  
Ring Structures ◽  
Aleutian Disease Of Mink ◽  
Aleutian Disease Virus ◽  
Disease Antigen

Aleutian disease of mink is transmissible by cell free extracts of affected mink tissues. Two antigenic components (Ag-1 and Ag-2) have been isolated from infected mink tissues by Kenyon and his associates. The relationships of the two antigens with the structural components of the Aleutian disease virus (ADV) have not yet been established; furthermore the details of the virus structure is lacking.We have prepared antigens from liver extracts of mink infected with Connecticut as well as Canadian strain of ADV. One of the antigen prepared from Connecticut strain of ADV contained primarily ring structures (13 nm in diameter) and few particules having icosahedral symmetry (27 nm in average diameter).

scholarly journals METABOLISM AND FUNCTION OF GAMMA GLOBULIN IN ALEUTIAN DISEASE OF MINK

1965 ◽  
Vol 121 (6) ◽  
pp. 889-900 ◽  
Author(s):  
David D. Porter ◽  
Frank J. Dixon ◽  
Austin E. Larsen
Keyword(s):  
Cell Proliferation ◽  
Gamma Globulin ◽  
Protein Complexes ◽  
Infectious Agent ◽  
Viral Agent ◽  
Vascular Changes ◽  
Glomerular Lesions ◽  
Aleutian Disease Of Mink ◽  
And Function ◽  
Aleutian Disease Virus

Aleutian disease-affected mink, which are markedly hypergammaglobulinemic, show a decreased half-life of the serum gamma globulin indicating that the hyperglobulinemia is due to increased production. No evidence that the gamma globulin was antibody to the infectious agent, to autologous or isologous tissues, or to antigens the animal was responding to prior to development of the disease was obtained. The increased gamma globulin was found to be of the 6.4S variety, and gamma globulin containing protein-protein complexes of 9S to 17S and 22S to 25S classes were observed in serums of affected mink. The findings are most consistent with the Aleutian disease virus acting as a direct and somewhat selective stimulus to plasma cell proliferation. There is no evidence that the arterial and glomerular lesions of Aleutian disease have an immunologic pathogenesis. It seems possible that these vascular changes may be directly caused by the viral agent, or may be the result of the increased gamma globulin levels.

scholarly journals THE PATHOGENESIS OF ALEUTIAN DISEASE OF MINK

1969 ◽  
Vol 130 (3) ◽  
pp. 575-593 ◽  
Author(s):  
David D. Porter ◽  
Austin E. Larsen ◽  
Helen G. Porter
Keyword(s):  
Disease Virus ◽  
Viral Antigen ◽  
Virus Disease ◽  
Virus Antigen ◽  
Slow Virus Disease ◽  
Infected Liver ◽  
Aleutian Disease Of Mink ◽  
Spleen And Lymph Nodes ◽  
High Virus ◽  
Aleutian Disease Virus

Mink inoculated with 1 x 105 ID50 of Aleutian disease virus revealed very high virus titers in the tissues 8–18 days later. The highest virus titers observed were 5 x 108 ID50 per g of spleen and 1 x 109 ID50 per g of liver 10 days after inoculation. Concomitant with the increase in infectious virus titers, viral antigen(s) was found in the cytoplasm of macrophages in the spleen and lymph nodes and in Kupffer cells in the liver. Antiviral antibody was assayed by indirect immunofluorescence, using sections of infected liver as the source of antigen. A few mink infected for 9 days and all those infected 10 days or more developed antibody to Aleutian disease virus antigen(s). By 60 days after infection, when hypergammaglobulinemia was marked, the mink had an exceptionally high mean antibody titer of 100,000. The pathogenesis of the glomerulonephritis of Aleutian disease is apparently related to formation of viral antigen-antibody-complement complexes which lodge in glomerular capillaries. No evidence was found that viral infection of the kidney took place, and no autoimmune responses were found. In this "slow-virus" disease the virus replicates rapidly and the morphologic and biochemical manifestations of disease are apparently due to the continuing interplay between a replicating antigen and the host immune response.

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