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.
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Boudewijns, R. et al. STAT2 signaling as double-edged sword restricting viral dissemination but driving severe pneumonia in SARS-CoV-2 infected hamsters. Preprint at bioRxiv https://doi.org/10.1101/2020.04.23.056838 (2020)
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Park, M.D. Type I and type III interferon in opposition?. Nat Rev Immunol 20, 406 (2020). https://doi.org/10.1038/s41577-020-0340-3
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DOI: https://doi.org/10.1038/s41577-020-0340-3