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  • Similarities and differences between severe COVID-19 pneumonia and anti-MDA-5-positive dermatomyositis-associated rapidly progressive interstitial lung diseases: a challenge for the future

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Correspondence
Similarities and differences between severe COVID-19 pneumonia and anti-MDA-5-positive dermatomyositis-associated rapidly progressive interstitial lung diseases: a challenge for the future
  1. Yukai Wang1,
  2. Guangzhou Du2,
  3. Guohong Zhang3,
  4. Marco Matucci-Cerinic4,
  5. Daniel E Furst5
  1. 1 Department of Rheumatology, Shantou Central Hospital, Shantou, Guangdong, China
  2. 2 Department of Radiology, Shantou Central Hospital, Shantou, Guangdong, China
  3. 3 Department of Pathology, Shantou University Medical College, Shantou, Guangdong, China
  4. 4 Department of Experimental and Clinical Medicine, University of Florence, Firenze, Toscana, Italy
  5. 5 Department of Rheumatology, University of California Los Angeles, Los Angeles, California, USA
  1. Correspondence to Dr Yukai Wang, Department of Rheumatology, Shantou Central Hospital, Shantou 515041, China; stzxyywyk{at}126.com

https://doi.org/10.1136/annrheumdis-2020-218594

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    We read with great interest the article by Megremis et al,1 who identified three immunogenic linear epitopes with high sequence identity to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) proteins in patients with dermatomyositis (DM). Speculatively, this finding could indicate that latent exposure to the Coronaviridae family might contribute to musculoskeletal autoimmune disease development.1 Consequently, SARS-CoV-2 infection might mimic myositis and could also lead to catastrophic results in patients with DM with prior interstitial lung disease (ILD) manifestation.

    COVID-19, caused by SARS-CoV-2, has rapidly spread to the whole world. Lung involvement is the hallmark of the disease, significantly associated with worse prognosis and higher mortality. The mechanism leading to acute lung injury in COVID-19 has not yet been completely elucidated. Nevertheless, immune dysfunction and cytokine dysregulation seem to play a pivotal role in this process. It is speculated that SARS-CoV-2 binds to target host cells through ACE 2, which is expressed in the airway and on type 2 pneumocytes in the lung. Subsequently, the virus triggers a storm of innate and adaptive immune response, resulting in the aberrant release of a large number of cytokines, including interleukin (IL)-1, IL-6, IL-10, granulocyte-macrophage colony stimulating factor (GM-CSF), monocyte …

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    Footnotes

    • Contributors YW wrote the manuscript. GD provided some evidences. GZ, DEF and MM-C revised the manuscript.

    • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

    • Competing interests None declared.

    • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

    • Provenance and peer review Not commissioned; internally peer reviewed.

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