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Inclusion body myositis: the mumps virus hypothesis
Abstract:
The resemblance of the filamentous inclusions in inclusion body myositis (IBM) to mumps virus nucleoproteins and the report of immunoreactivity of the inclusions for mumps virus antigens have implicated the mumps virus in the etiology of IBM. We tested the mumps virus hypothesis by in-situ hybridization with a cDNA probe specific for the mumps virus nucleocapsid gene, and immunocytochemically with antibodies against "soluble" and "viral" mumps antigens. The tests were performed on muscle specimens (IBM, 20; acid maltase deficiency, 4; chloroquine myopathy, 2; nonweak control subjects, 5) and mumps virus-infected and uninfected HEp-2 cells. The in-situ hybridization study showed a strong specific signal in the infected HEp-2 cells but no specific signal in IBM, other myopathies, or nonweak control subjects. The immunocytochemical study showed specific binding of the antimumps antibodies to the infected HEp-2 cells but demonstrated only nonspecific binding of these antibodies around rimmed vacuoles in IBM, acid maltase deficiency, and chloroquine myopathy. These studies cast doubt on the mumps hypothesis of IBM.
Insights
This study investigated the mumps virus hypothesis for inclusion body myositis (IBM). Researchers found no evidence of mumps virus in IBM muscle tissue, questioning its role in the disease.
Area of Science:
- Neurology
- Virology
- Molecular Biology
Background:
- Filamentous inclusions in inclusion body myositis (IBM) resemble mumps virus nucleoproteins.
- Previous reports suggested immunoreactivity with mumps virus antigens, implicating the virus in IBM etiology.
Purpose of the Study:
- To investigate the hypothesis that mumps virus is involved in the cause of inclusion body myositis (IBM).
- To evaluate the presence of mumps virus in muscle tissue from IBM patients and controls.
Main Methods:
- In-situ hybridization using a specific cDNA probe for the mumps virus nucleocapsid gene.
- Immunocytochemical analysis with antibodies against mumps virus antigens.
- Testing on muscle specimens from IBM patients, other myopathies, and control subjects, alongside mumps virus-infected and uninfected HEp-2 cells.
Main Results:
- In-situ hybridization showed a strong, specific signal in mumps virus-infected cells but no specific signal in IBM or control muscle tissue.
- Immunocytochemistry revealed specific binding in infected cells, but only non-specific binding around rimmed vacuoles in IBM and other myopathy specimens.
Conclusions:
- The findings cast doubt on the mumps virus hypothesis for the etiology of inclusion body myositis (IBM).
- Neither molecular nor immunocytochemical evidence supported the presence of mumps virus in IBM muscle.