Most reports of influenza virus-induced myositis describe cases in children; however, cases in adults are known to occur. Most cases are caused by the influenza A and B virus, and the condition is typically referred to as sporadic acute benign myositis (Capoferri, 2018). The main symptom is pain in the muscles of the posterior compartment of the calves (the gastrocnemius and soleus muscles). It often causes difficulty in rising and walking and is more common in boys than in girls. Prognosis is generally good, and recovery occurs within a week.
Sporadic acute benign myositis is also observed in paramyxovirus infection. Paramyxovirus has long been hypothesized as a cause of inclusion body myositis, although the virus has not been isolated from muscle specimens.
Human immunodeficiency virus (HIV) and human T-lymphotrophic virus type 1 (HTLV-1) can cause inflammatory myopathy in humans.
Histopathological findings in muscle tissue of patients with HIV infection include a wide variety of changes including polymyositis (PM), dermatomyositis (DM), non-specific myositis (NM), isolated mitochondrial abnormality (IMA), immunemediated necrotizing myopathy (IMNM), and inclusion body myositis (IBM). Previous studies have reported that a small number of patients showed nemaline rods in the muscle and a few others showed neuropathic changes probably secondary to a motor neuron disease-like change. It should be noted that some of these patients were co-infected with hepatitis B or hepatitis C viruses and were also treated with zidovudine and other drugs known to cause myopathy.
Histopathological features of PM and IBM that are observed in patients with HIV infection are indistinguishable from those observed in sporadic cases without infection. Similarly, immnohistochemical features such as aberrant expression of the MHC class I antigen on the muscle cell surface and CD8+ cell infiltration in the plasma membrane of the muscle cells are also common between these conditions. However, the HIV virus has not been observed in the muscle tissue except within the infiltrating lymphocytes.
Landon-Cardinal et al. (2019) reported evaluation of muscle biopsy specimens in 50 patients. Following findings were observed among 46 patients who showed histopathological abnormalities: 39% PM (18/46), 26% NSM (12/46), 26% IMA (12/46), 7% IBM (3/46), and 2% IMNM (1/46). Furthermore, among 7 patients with PM who underwent re-biopsy of the muscle, 3 were shown to have developed IBM. Clinically, about 50% of the patients who were initially diagnosed as PM developed symptoms compatible with IBM within a mean duration of 2.3 years, based on the European Neuromuscular Center criteria. This report highlights the association between IBM and PM and the clinical implications of this observation.
HTLV-1 is known to cause tropical spastic paraplegia and HTLV-1–associated myelopathy (HAM). PM and IBM may occur in association with these conditions or independently. Myositis-induced morbidity is significantly higher in people infected with HTLV-1 than in the non-infected population in southern Japan and the Caribbean. Histopathological features of myositis are identical in these populations. To date, the virus has not been observed in the muscle tissue except within the infiltrating lymphocytes.
Myositis caused by enterovirus infections including the coxsackie virus has been reported in a few cases. However, the virus has not been observed within muscle tissue.
Hepatitis C virus is known to cause cryoglobulinemia associated with vasculitis and neuropathy. Cases of PM (Villanova, 2000), DM, and IBM (Warabi, 2004; Uruha, 2016） have been reported. Notably, the virus has not been observed in muscle tissue samples.
