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SARS-CoV-2 infected cells trigger an acute antiviral response mediated by Plasmacytoid dendritic cells in mild but not severe COVID-19 patients

Venet, M.; Sa Ribeiro, M.; Decembre, E.; Bellomo, A.; Joshi, G.; Villard, M.; Cluet, D.; Perret, M.; Pescamona, R.; Paidassi, H.; Walzer, T.; Allatif, O.; Belot, A.; trouillet-assant, S.; Ricci, E.; DREUX, M.

2021-09-08 infectious diseases
10.1101/2021.09.01.21262969 medRxiv
Show abstract

Type I and III interferons (IFN-I/{lambda}) are key antiviral mediators against SARS-CoV-2 infection. Here, we demonstrate that plasmacytoid dendritic cells (pDCs) are the predominant IFN-I/{lambda} source following their sensing of SARS-CoV-2-infected cells. Mechanistically, this short-range sensing by pDCs requires sustained integrin-mediated cell adhesion with infected cells. In turn, pDCs restrict viral spread by an IFN-I/{lambda} response directed toward SARS-CoV-2-infected cells. This specialized function enables pDCs to efficiently turn-off viral replication, likely via a local response at the contact site with infected cells. By exploring the pDC response in SARS-CoV-2 patients, we further demonstrate that pDC responsiveness inversely correlates with the severity of the disease. The pDC response is particularly impaired in severe COVID-19 patients. Overall, we propose that pDC activation is essential to control SARS-CoV-2-infection. Failure to unfold this response could be key to understand severe cases of COVID-19.

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