In this preprint, Boudewijns et al. examined the interferon (IFN) response in Syrian hamsters, which develop significant lung pathology after SARS-CoV-2 infection, and in C57BL/6 mice, which do not. However, SARS-CoV-2-infected Ifnar1 mice had an increased infiltration of inflammatory cells in the lung, suggesting that an active, functional and immediate type I IFN response restricts pathogenesis in mice. The analysis of hamsters with a deletion of Stat2 (which causes a loss of type I and type III IFN signalling) or of Il28r (resulting in loss of type III IFN signalling alone) suggested that type III IFNs help to restrict viral dissemination, whereas type I IFNs exacerbate bronchopneumonia in hamsters. These opposing roles warrant further study, and the histological findings suggest that the Syrian hamster is a better model for COVID-19 than the mouse.
Authors: Robbert Boudewijns; Hendrik Jan Thibaut; Suzanne J F Kaptein; Rong Li; Valentijn Vergote; Laura Seldeslachts; Johan Van Weyenbergh; Carolien De Keyzer; Lindsey Bervoets; Sapna Sharma; Laurens Liesenborghs; Ji Ma; Sander Jansen; Dominique Van Looveren; Thomas Vercruysse; Xinyu Wang; Dirk Jochmans; Erik Martens; Kenny Roose; Dorien De Vlieger; Bert Schepens; Tina Van Buyten; Sofie Jacobs; Yanan Liu; Joan Martí-Carreras; Bert Vanmechelen; Tony Wawina-Bokalanga; Leen Delang; Joana Rocha-Pereira; Lotte Coelmont; Winston Chiu; Pieter Leyssen; Elisabeth Heylen; Dominique Schols; Lanjiao Wang; Lila Close; Jelle Matthijnssens; Marc Van Ranst; Veerle Compernolle; Georg Schramm; Koen Van Laere; Xavier Saelens; Nico Callewaert; Ghislain Opdenakker; Piet Maes; Birgit Weynand; Christopher Cawthorne; Greetje Vande Velde; Zhongde Wang; Johan Neyts; Kai Dallmeier Journal: Nat Commun Date: 2020-11-17 Impact factor: 14.919