Experimental influenza B viral myositis.

To investigate the pathogenesis of influenza myositis in animals, juvenile BALB/c mice were inoculated with influenza B/Lee virus intramuscularly into the right quadriceps muscle. Chicken normal allantoic fluid (NAF) or phosphate-buffered saline (PBS) was injected into the left quadriceps of control mice and in some virus-infected mice. Serum creatinine phosphokinase (CPK) levels rose significantly on days 1 and 2 post-inoculation (PI) in only virus-inoculated mice. On days 2 and 3 PI, right quadriceps muscles developed scattered foci of a predominantly mononuclear inflammation in the perimysial connective tissue often adjacent to degenerating or necrotic muscle fibers. Immunofluorescent staining with specific anti-influenza B virus antisera showed muscle fibers that contained specific staining in nuclei and adjacent cytoplasm. Skip areas of staining within muscle fibers suggested that not all muscle nuclei within an individual muscle fiber were infected. A continuous fall in infectious virus titer in the right quadriceps muscles suggested the initial virus inoculum became inactivated and progeny virions were not produced. Left quadriceps muscle never had muscle necrosis or endomysial inflammation, specific staining of viral antigen, virus isolation, or viral RNA detected by the reverse transcriptase polymerase chain reaction assay. These findings support the hypothesis that a non-permissive influenza viral infection can develop in murine skeletal muscle that can damage specific nuclear domains of muscle fibers producing muscle degeneration or necrosis. A similar type of muscle infection may develop in humans that occasionally develop focal myositis during influenza.