Author:
Aschman Tom,Wyler Emanuel,Baum Oliver,Hentschel Andreas,Legler Franziska,Preusse Corinna,Meyer-Arndt Lil,Büttnerova Ivana,Förster Alexandra,Cengiz Derya,Teixeira Alves Luiz Gustavo,Schneider Julia,Kedor Claudia,Rust Rebecca,Bellmann-Strobl Judith,Aminaa Sanchin,Vajkoczy Peter,Goebel Hans-Hilmar,Landthaler Markus,Corman Victor,Roos Andreas,Heppner Frank L.,Radbruch Helena,Paul Friedemann,Scheibenbogen Carmen,Stenzel Werner,Dengler Nora F.
Abstract
AbstractThe SARS-CoV-2 pandemic not only resulted in millions of acute infections worldwide, but also caused innumerable cases of post-infectious syndromes, colloquially referred to as “long COVID”. Due to the heterogeneous nature of symptoms and scarcity of available tissue samples, little is known about the underlying mechanisms. We present an in-depth analysis of skeletal muscle biopsies obtained from eleven patients suffering from enduring fatigue and post-exertional malaise after an infection with SARS-CoV-2. Compared to two independent historical control cohorts, patients with post-COVID exertion intolerance had fewer capillaries, thicker capillary basement membranes and increased numbers of CD169+macrophages. SARS-CoV-2 RNA could not be detected in the muscle tissues, but transcriptomic analysis revealed distinct gene signatures compared to the two control cohorts, indicating immune dysregulations and altered metabolic pathways. We hypothesize that the initial viral infection may have caused immune-mediated structural changes of the microvasculature, potentially explaining the exercise-dependent fatigue and muscle pain.
Publisher
Cold Spring Harbor Laboratory
Cited by
1 articles.
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