Mitogen- and viral antigen-induced transformation of lymphocytes from normal mink and from mink with progressive or nonprogressive Aleutian disease.
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Peripheral blood lymphocytes (PBL) from mink with progressive Aleutian disease (AD) were shown to be significantly less responsive to phytohemagglutinin, concanavalin A, and pokeweed mitogen than were PBL from normal mink and from mink with a nonprogressive form of AD. Response to the virus of AD was significantly greater in PBL cultures from mink with nonprogressive AD than in those from normal mink or mink with progressive AD. After experimental infection with AD virus, mink PBL were responsive to viral antigen only transiently. These findings suggest that lymphocyte responsiveness as indicated by transformation induced by mitogens or viral antigen may be an important aspect of host response to infection with the parvovirus of AD. (+info)
Identification of a nonvirion protein of Aleutian disease virus: mink with Aleutian disease have antibody to both virion and nonvirion proteins.
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We studied Aleutian disease virus polypeptides in Crandall feline kidney (CRFK) cells. When CRFK cells labeled with [35S]methionine at 60 h postinfection were studied by immunoprecipitation with sera from infected mink, the major Aleutian disease virus virion polypeptides (p85 and p75) were consistently identified, as was a 71,000-dalton nonvirion protein (p71). The peptide maps of p85 and p75 were similar, but the map of p71 was different. p85, p75, and p71 were all precipitated by sera from Aleutian disease virus-infected mink, including those with signs of progressive disease, but heterologous sera raised against purified Aleutian disease virus did not precipitate the nonvirion p71. These results indicated that the nonvirion p71 was unrelated to p85 and p75 and further suggested that mink infected with Aleutian disease virus develop antibody to nonvirion, as well as structural, viral proteins. (+info)
Immunoglobulin classes of Aleutian disease virus antibody.
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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. (+info)
Ocular lesions in mink affected with Aleutian disease.
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Uveitis, characterized by infiltrates of lymphocytes and plasma cells, was the principal ocular lesion in 122 sapphire and pastel mink affected with experimental Aleutian disease. It was present to various degrees in all but five mink examined five to 164 weeks after inoculation (intraperitoneal or intranasal) with any of four North American strains of Aleutian disease virus. The uveitis, mostly iridocyclitis, was accompanied often by protein-rich fluid in the anterior chamber and less often by fibrin and cells in the vitreous body. Cellular infiltration of the limbus, seldom pronounced, also occurred in about 20% of the mink. In 11 mink with moderate or severe uveitis, the retina was detached by pools of protein-rich fluid. Infiltrates of lymphocytes, plasma cells, and a few histiocytes often were found in the orbital soft tissues, occasionally in association with retrobulbar arteritis. In general, the ocular lesions were more severe in sapphire than in pastel mink. The uveitis accompanies glomerulonephritis, the principal lesion of Aleutian disease, much more regularly than do several other lesions of the disease. Like the glomerulonephritis, it probably results from the deposition of circulating immune complexes. (+info)
Expression of Aleutian mink disease parvovirus capsid proteins in a baculovirus expression system for potential diagnostic use.
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A 2.3-kb cDNA clone encoding Aleutian mink disease parvovirus (ADV) structural proteins VP1 and VP2 was inserted into the polyhedron gene of Autographa californica nuclear polyhedrosis virus (AcNPV) and expressed by the recombinant virus, AcADV-1, in Spodoptera frugiperda-9 cells. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis and western immunoblot analysis (WIA) indicated that synthesis of both VP1 and VP2 was being directed by AcADV-1. Fluorescence microscopic examination of AcADV-1-infected S. frugiperda-9 cells indicated that the recombinant protein was present within the nucleus of the cells, and electron microscopic examination of these cells revealed the presence of small particles 23-25 nm in diameter. Structures resembling empty ADV capsids could be purified on CsCl density gradients, thus indicating that the ADV proteins were self-assembling. The antigenicity of recombinant VP1 and VP2 was evaluated by WIA. Sera collected from 16 mink prior to infection with ADV did not react with VP1 and VP2. Ten sera collected from mink with counter current immunoelectrophoresis (CIE) titers greater than 4 (log2) reacted with VP1 and VP2 in WIA. Two of 6 sera with CIE titers of 4 and 1 of 14 sera with CIE titers < 4 reacted with the recombinant proteins. These results suggest that baculovirus recombinant ADV capsid proteins may be useful as diagnostic antigens. (+info)
Pathogenesis of aleutian disease of mink: identification of nonpersistent infections.
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Aleutian disease virus usually produces a persistent infection and progressive immune comples disease in mink of the Aleutian genotype. Study of Aleutian disease virus infection in non-Aleutian mink showed that about one-quarter developed nonpersistent infections by the virus, and that the nonpersistence was not genetically determined by the host. The nonpersistently infected mink developed only a transient elevation of serum gamma globulin, and much lower specific Aleutian disease virus antibody titers than persistently infected mink. No lesions were found in the nonpersistently infected mink. (+info)
Role of alveolar type II cells and of surfactant-associated protein C mRNA levels in the pathogenesis of respiratory distress in mink kits infected with Aleutian mink disease parvovirus.
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Neonatal mink kits infected with Aleutian mink disease parvovirus (ADV) develop an acute interstitial pneumonia with clinical symptoms and pathological lesions that resemble those seen in preterm human infants with respiratory distress syndrome and in human adults with adult respiratory distress syndrome. We have previously suggested that ADV replicates in the alveolar type II epithelial cells of the lung. By using double in situ hybridization, with the simultaneous use of a probe to detect ADV replication and a probe to demonstrate alveolar type II cells, we now confirm this hypothesis. Furthermore, Northern (RNA) blot hybridization showed that the infection caused a significant decrease of surfactant-associated protein C mRNA produced by the alveolar type II cells. We therefore suggest that the severe clinical symptoms and pathological changes characterized by hyaline membrane formation observed in ADV-infected mink kits are caused by a dysfunction of alveolar surfactant similar to that observed in respiratory distress syndrome in preterm infants. However, in the infected mink kits the dysfunction is due to the replication of ADV in the lungs, whereas the dysfunction of surfactant in preterm infants is due to lung immaturity. (+info)
Interstitial nephritis in Aleutian mink disease. Possible role of cell-mediated immunity against virus-infected tubular epithelial cells.
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Aleutian mink disease (AD) has been characterized by immune complex glomerulonephritis associated with persistent infection of Aleutian mink disease parvovirus (ADV). Histopathological examination of kidneys from ADV-infected mink in this study revealed that interstitial nephritis characterized by prominent damage of renal tubuli and lymphocyte infiltration was also common in AD along with glomerulonephritis. By using strand-specific in situ molecular hybridization technique, replication of ADV was observed in tubular epithelial cells, in addition to epithelial cells of Bowman's capsules and some glomerular cells of the infected mink. Analysis of tubular lesions by a combination of immunohistochemistry and in situ hybridization revealed that the renal tubuli positive for virion DNA or replicative form DNA/mRNA of ADV were also positive for an activation marker of immunocompetent cells, which is shared by B lymphocytes and thymic epithelial cells. Infiltration of a subpopulation of T lymphocytes around infected renal tubuli were observed but deposition of immune complexes in these tubular lesions was not demonstrable. ADV replication in epithelial cells of renal tubuli and cell-mediated immune responses to the infected epithelial cells may play a role in the pathogenesis of interstitial nephritis in Aleutian mink disease. (+info)