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Myopathy associated with SARS-CoV-2 infection is likely a postviral phenomenon, new research suggests.

“The findings of this study strongly suggest that there is a postinfectious myopathy in a subset of patients who were infected with SARS-CoV-2, which potentially can explain the muscle problems in long-COVID or post-COVID,” Tom Aschman, MD, with the Department of Neuropathology, Charité-Universitätsmedizin Berlin, Berlin, Germany, told Medscape Medical News.

The study was published online June 11 in JAMA Neurology.

Blame the Immune System

Muscle pain and weakness, often associated with elevations in creatine kinase, a marker of skeletal muscle injury, have been reported in patients with COVID-19, particularly those with more severe illness. However, muscle biopsies are rarely performed in suspected cases of virus-associated myositis.

The investigators assessed skeletal muscle samples from 43 adults who died with severe COVID-19 and compared them with specimens from 11 adults without COVID-19 who died of other critical illnesses.

The median age of case patients who died with COVID-19 was 72 years, and 72% were men. The median age of the control patients was 71 years, and 64% were men.

Skeletal muscle samples from the COVID-19 patients showed a significantly higher overall pathology (P < .001) and inflammation score (P < .001). Signs of degenerating muscle fibers were also more common in the COVID-19 cohort (P < .005).

Most of the COVID-19 patients showed signs of myositis, ranging from mild to severe, the authors report.

Inflammation of skeletal muscles was associated with the duration of illness and was more pronounced than cardiac inflammation. In some muscle specimens, SARS-CoV-2 RNA was detected by reverse transcription–polymerase chain reaction, but there was no evidence of direct invasion of SARS-CoV-2 in muscle tissue.

Clinically significant expression of MHC class I antigens on the sarcolemma was observed in 23 of 42 COVID-19 specimens (55%); upregulation of MHC class II antigens was found in seven of 42 specimens (17%). Neither were found in any of the control specimens.

“Significant upregulation of MHC class I antigens in the early phase of the disease and concomitant upregulation of MHC class II antigens on myofibers in later stages indicate involvement of skeletal muscle in the immune response against SARS-CoV-2,” the researchers write.

Overall, they believe the findings support an immune-mediated myopathy rather than a direct viral infection of myofibers.

They also observed that necrotic myofibers and capillary complement deposition were not confined to muscles of patients with COVID-19, suggesting that these findings are not specific to COVID-19 but rather are consequences of sepsis and/or critical illness.

“The take-home message for clinicians,” said Aschman, “is that patients with severe COVID-19 often suffer from inflammation of skeletal muscles (myositis), which could explain elevated levels of creatine kinase (CK) and muscle pain and weakness.”

An important caveat is that the study was restricted to COVID-19 patients with severe disease who had a fatal outcome. This limits extrapolation to patients with mild SARS-CoV-2 infection. In addition, data on clinical correlates (myalgia, myopathy) before death were scarce.

“Whether these findings can be extrapolated to milder disease courses and potentially explain chronic muscle fatigue syndromes as described in post-acute COVID-19 syndromes and whether autoimmune mechanisms are involved will need to be addressed in future studies,” the researchers write.

The research was supported by the European Union’s Horizon 2020 research and innovation program through RECOVER, the German Ministry of Health and the German Federal Ministry of Education and Research. The authors’ disclosures of relevant financial relationships are listed in the original article.

JAMA Neurol. Published online June 11, 2021. Full text

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