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© Research
Publication : bioRxiv

Syncytia formation by SARS-CoV-2 infected cells

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in bioRxiv - 14 Jul 2020

Buchrieser, J. Dufloo, M. Hubert, B. Monel, D. Planas, M. M. Rajah, C. Planchais, F. Porrot, F. Guivel-Benhassine, S. Van der Werf, N. Casartelli, H. Mouquet, T. Bruel, O. Schwartz

Link to DOI [DOI] – 10.1101/2020.07.14.202028

Severe cases of COVID-19 are associated with extensive lung damage and the presence of infected multinucleated syncytial pneumocytes. The viral and cellular mechanisms regulating the formation of these syncytia are not well understood. Here, we show that SARS-CoV-2 infected cells express the viral Spike protein (S) at their surface and fuse with ACE2-positive neighbouring cells. Expression of S without any other viral proteins triggers syncytia formation. Type-I interferon (IFN)-induced transmembrane proteins (IFITMs), a family of restriction factors that block the entry of many viruses, inhibit S-mediated fusion, with IFITM1 being more active than IFITM2 and IFITM3. On the contrary, the TMPRSS2 serine protease, which is known to enhance infectivity of cell-free virions, processes both S and ACE2 and increases syncytia formation by accelerating the fusion process. TMPRSS2 thwarts the antiviral effect of IFITMs. Our results show that the pathological effects of SARS-CoV-2 are modulated by cellular proteins that either inhibit or facilitate syncytia formation.

https://www.biorxiv.org/content/10.1101/2020.07.14.202028v1