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. 2022 Mar 18;13:813924. doi: 10.3389/fphys.2022.813924

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Copyright © 2022 dos Santos, Sigoli, Bragança and Cornachione.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Mechanisms of action of SARS-CoV-2 on the skeletal muscle tissue. (A) Direct mechanism via SARS-CoV-2 binding to receptors on the skeletal muscle cell surface and entry of the virus into the cell. Several types of musculoskeletal cells express ACE2 and/or TMPRSS2, which allows this type of direct mechanism of action of the virus. (B) Indirect mechanism considering the adverse effects of the elevated inflammatory process (“cytokine storm”) caused by SARS-CoV-2 infection on the musculoskeletal tissue. The deregulated release of cytokines and chemokines (IL-6, IL-1β, IL-8, IFN-γ, IP-10, TNF-α) by the immune system results in exacerbated inflammation that can lead to multi-organ injuries. Both mechanisms (A,B) can affect the musculoskeletal system, causing manifestations such as fatigue and myalgia in symptomatic COVID-19 individuals. ACE2: angiotensin-converting enzyme 2; IFN-γ: interferon-gamma; IL-1β: interleukin-1β; IL-6: interleukin-6; IL-8: interleukin-8; IP-10: interferon-gamma inducible protein 10; TMPRSS2: transmembrane protease serine 2; TNF-α: tumor necrosis factor alpha.