Key result
Aleutian disease virus infection in mink causes marked hypergammaglobulinemia primarily due to IgG, with an early transient IgM response and a late marked elevation of IgA.
ADV infection in mink induces a specific temporal pattern of immunoglobulin class responses, predominantly IgG, with early IgM and elevated IgA.
Provides mink model of viral Ig class kinetics; hypothesis-generating for human responses but leaves open clinical relevance.
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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Porter et al. (1984) studied Aleutian disease virus infection (n=161). Aleutian disease virus (ADV) infection vs. Uninfected mink was evaluated on Serum immunoglobulin levels (IgG, IgM, IgA) and ADV-specific antibodies. Aleutian disease virus infection in mink causes marked hypergammaglobulinemia primarily due to IgG, with an early transient IgM response and a late marked elevation of IgA.
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