NEW YORK (Reuters Health) – The muscle damage sometimes seen with COVID-19 appears to be due to the immune response, not to direct invasion of muscle tissue by the virus, a new autopsy series suggests.
“While it is not uncommon to experience muscle pain during other viral illnesses, the exact reason for this remained unclear,” said lead author Dr. Tom Aschman of Freie Universitat Berlin and Humboldt-Universitat zu Berlin, in Germany. “Knowing that muscle problems are due to an overactive immune system rather than penetration by viral particles opens up potential immunosuppressive or immune-modulating therapy options.”
“The most important finding of our study is that severe COVID-19 can be accompanied by an immune-mediated myositis, explaining elevated muscle enzymes and muscle pain and/or weakness,” he told Reuters Health by email. “Skeletal muscle inflammation was increased in chronically ill patients and in general was more severe than cardiac muscle inflammation.”
As reported in JAMA Neurology, Dr. Aschman and his colleagues conducted postmortem analyses of skeletal muscle and myocardial inflammation in patients who had died over one year and had been autopsied.
The team compared samples from 43 individuals diagnosed with SARS-CoV-2 infection by PCR tests and clinical findings suggestive of COVID-19 with samples from 11 individuals whose PCR tests were negative and who had no clinical signs of COVID-19.
Among individuals with COVID-19, the authors detected clinically significant expression of MHC class I antigens on the sarcolemma in 23 of 42 (55%) specimens, as well as upregulation of MHC class II antigens in seven specimens (17%). Neither was present in any of the controls.
Specimens from COVID-19 patients also displayed higher numbers of natural killer cells (median, eight cells vs. three cells per 10 high-power fields; P<0.001).
Skeletal muscle from the individuals who died with COVID-19 had a higher overall pathology score (mean, 3.4 vs. 1.5, P<0.001) as well as a higher inflammation score (3.5 vs. 1.0, P<0.001).
Skeletal muscles displayed more inflammatory features than cardiac muscle, and inflammation was greatest in patients whose COVID-19 ran a chronic course; however, the researchers found no evidence of direct muscle-tissue infection.
“The number of severely ill COVID-19 patients who showed signs of inflammatory myopathy surprised me,” Dr. Aschman said.
“Whether these findings can be extrapolated to milder disease courses and potentially explain chronic muscle fatigue syndromes as described in postacute COVID-19 syndromes and whether autoimmune mechanisms are involved will need to be addressed in future studies,” he and his colleagues write.
Dr. Aschman said one strength of the study is its control group of critically ill but SARS-CoV-2-negative patients. “This allows us to avoid a bias through effects of critical illness in general on muscle tissue.”
He acknowledged that “one study weakness is that we can’t tell if the effects observed are specific to viral infections or to SARS-CoV-2.”
SOURCE: https://bit.ly/2Uqmq3z JAMA Neurology, online June 11, 2021.
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