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.