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Vimentin as a target for the treatment of COVID-19
  1. Zhenlin Li1,
  2. Denise Paulin1,
  3. Patrick Lacolley2,
  4. Dario Coletti1,3 and
  5. Onnik Agbulut1
  1. 1Biological Adaptation and Ageing, CNRS UMR 8256, Inserm U1164, Sorbonne Université, Institut de Biologie Paris-Seine, Paris, France
  2. 2Inserm, UMR_S 1116, DCAC, Université de Lorraine, Nancy, Lorraine, France
  3. 3Department of Anatomy, Histology, Forensic Medicine & Orthopedics, Histology & Medical Embryology Section, Sapienza University of Rome, Roma, Lazio, Italy
  1. Correspondence to Professor Onnik Agbulut; onnik.agbulut{at}


We and others propose vimentin as a possible cellular target for the treatment of COVID-19. This innovative idea is so recent that it requires further attention and debate. The significant role played by vimentin in virus-induced infection however is well established: (1) vimentin has been reported as a co-receptor and/or attachment site for SARS-CoV; (2) vimentin is involved in viral replication in cells; (3) vimentin plays a fundamental role in both the viral infection and the consequent explosive immune-inflammatory response and (4) a lower vimentin expression is associated with the inhibition of epithelial to mesenchymal transition and fibrosis. Moreover, the absence of vimentin in mice makes them resistant to lung injury. Since vimentin has a twofold role in the disease, not only being involved in the viral infection but also in the associated life-threatening lung inflammation, the use of vimentin-targeted drugs may offer a synergistic advantage as compared with other treatments not targeting vimentin. Consequently, we speculate here that drugs which decrease the expression of vimentin can be used for the treatment of patients with COVID-19 and advise that several Food and Drug Administration-approved drugs be immediately tested in clinical trials against SARS-CoV-2, thus broadening therapeutic options for this type of viral infection.

  • pneumonia
  • viral infection
  • respiratory infection
  • ARDS

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  • Contributors ZL and OA developed the idea, wrote the first draft and are the guarantors of the article jointly. DC and OA expanded and fine-tuned the original version of the paper. DP and PL provided their expertise to give further depth to the review of the literature the manuscript is based on.

  • Funding This research was partly supported by Sorbonne Université, INSERM, CNRS. ZL and OA are supported by the AFM-Téléthon (contract numbers: 21833 and 22142) and the Fédération Française de Cardiologie. DC is supported by Sapienza University Ateneo 2019 and the AFM-Téléthon (contract number: 20603).

  • Competing interests None declared.

  • Patient consent for publication Not required.

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

  • Data availability statement All data relevant to the study are included in the article or uploaded as supplementary information. All data relevant to the study are included in the article.

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