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. 1969 Sep 1;130(3):575–593. doi: 10.1084/jem.130.3.575

THE PATHOGENESIS OF ALEUTIAN DISEASE OF MINK

I. IN VIVO VIRAL REPLICATION AND THE HOST ANTIBODY RESPONSE TO VIRAL ANTIGEN

David D Porter 1, Austin E Larsen 1, Helen G Porter 1
PMCID: PMC2138710  PMID: 4979953

Abstract

Mink inoculated with 1 x 105 ID 50 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 ID 50 per g of spleen and 1 x 109 ID 50 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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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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