Immunologic and Genetic Aspects of Aleutian Disease

Lodmell, Donald L.; Portis, John L.

doi:10.1007/978-1-4684-8652-0_3

Cited by 20 publications

(15 citation statements)

References 107 publications

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“…Certainly susceptibility or resistance of pastel mink to AD does not have a simple genetic explanation (15,20). And despite the profound constitutional differences between pastel and sapphire mink attributable to the pleiotropic effects of the Aleutian gene in sapphire mink (18,19,24), the basis for the generally greater susceptibility of sapphire mink to AD is not understood (21).…”

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confidence: 99%

Comparative pathogenicity of four strains of Aleutian disease virus for pastel and sapphire mink

Hadlow¹,

Race²,

Kennedy³

1983

Infect Immun

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Information was sought on the comparative pathogenicity of four North American strains (isolates) of Aleutian disease virus for royal pastel (a non-Aleutian genotype) and sapphire (an Aleutian gejnotype) mink. The four strains (Utah-1, Ontario [Canada], Montana, and Pullman [Washington]), all of mink origin, were inoculated intraperitoneally and intranasally in serial 10-fold dilutions. As indicated by the appearance of specific antibody (counterimmunoelectrophoresis test), all strains readily infected both color phases of mink, and all strains were equally pathogenic for sapphire mink. Not all strains, however, regularly caused Aleutian disease in pastel mink. Infection of pastel mink with the Utah-1 strain invariably led to fatal disease. Infection with the Ontario strain caused fatal disease nearly as often. The Pullman strain, by contrast, almost never caused disease in infected pastel mink. The pathogenicity of the Montana strain for this color phase was between these extremes. These findings emphasize the need to distinguish between infection and disease when mink are exposed to Aleutian disease virus. The distinction has important implications for understanding the natural history of Aleutian disease virus infection in ranch mink.

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Section: 'mentioning

confidence: 99%

Comparative pathogenicity of four strains of Aleutian disease virus for pastel and sapphire mink

Hadlow¹,

Race²,

Kennedy³

1983

Infect Immun

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“…Aleutian disease (AD) is a naturally occurring disease of ranch mink (Mustela vison) caused by a nondefective parvovirus (7,38). AD is characterized by persistent viremia, hypergammaglobulinemia, plasmacytosis, and immune complex-mediated vasculitis and glomerulonephritis (15,28,32,34). Mink genotypes differ in susceptibility to AD.…”

mentioning

confidence: 99%

Interferon response in normal and Aleutian disease virus-infected mink

Wiedbrauk¹,

Hadlow²,

Ewalt³

et al. 1986

J Virol

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Studies were done to determine whether differences in interferon production are responsible for the resistance of pastel mink to Aleutian disease. The abilities of normal pastel and sapphire mink to produce interferon when inoculated with either Newcastle disease virus or a synthetic polyribonucleotide, poly (I):poly (C), were identical, even to the production of a novel, acid-labile interferon. The resistance of pastel mink to Aleutian disease did not correlate with interferon production, because neither sapphire nor pastel mink produced detectable amounts of interferon when infected with either the Pullman strain of Aleutian disease virus (ADV) or the highly virulent Utah I strain. Sapphire mink infected with the Pullman strain responded normally to poly (I):poly (C) early in the course of the disease, but interferon production was impaired late, when the mink were hypergammaglobulinemic and had renal, vascular, and hepatic lesions. These data suggest that ADV Pullman neither stimulates nor interferes with interferon production in infected mink and may represent a mechanism whereby ADV can more readily establish infection.

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“…Aleutian disease virus (ADV) is an autonomous parvovirus (3,29). Mink with AD develop a systemic plasmacytosis with markedly increased serum gamma globulin, and glomerulonephritis and arteritis are caused by tissue deposition of immune complexes (reviewed in references 21 and 31). The striking elevation of gamma globulin in AD has been shown to be caused by overproduction of immunoglobulin G (IgG) (28).…”

mentioning

confidence: 99%

Immunoglobulin classes of Aleutian disease virus antibody

Porter¹,

Porter²,

Suffin³

et al. 1984

Infect Immun

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Aleutian disease virus (ADV) persistently infects mink and causes marked hypergammaglobulinemia. Immunoglobulin class-specific antisera were used to define the total immunoglobulin of each class by radial immunodiffusion and the immunoglobulin class of ADV-specific antibody by immunofluorescence in experimentally and naturally infected mink. Electrophoretic gamma globulin closely reflects the immunoglobulin G (IgG) level in mink, and the majority of the increased immunoglobulin and ADV antibody in infected mink is IgG. IgM becomes elevated within 6 days after infection, reaches peak levels by 15 to 18 days, and returns to normal by 60 days after infection. The first ADV antibody demonstrable is IgM, and most mink have virus-specific IgM antibody for at least 85 days postinfection. Serum IgA levels in normal mink are not normally distributed, and ADV infection causes a marked elevation of IgA. Low levels of ADV-specific IgA antibody can be shown throughout the course of infection. Failure of large amounts of virus-specific IgG antibody to inhibit the reaction of virus-specific IgM and IgA antibodies suggests that the various classes of antibodies are directed against spatially different antigenic determinants. The IgM and IgA were shown not to be rheumatoid factors.

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Immunologic and Genetic Aspects of Aleutian Disease

Cited by 20 publications

References 107 publications

Comparative pathogenicity of four strains of Aleutian disease virus for pastel and sapphire mink

Comparative pathogenicity of four strains of Aleutian disease virus for pastel and sapphire mink

Interferon response in normal and Aleutian disease virus-infected mink

Immunoglobulin classes of Aleutian disease virus antibody

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