Journal
NATURE COMMUNICATIONS
Volume 11, Issue 1, Pages -Publisher
NATURE PORTFOLIO
DOI: 10.1038/s41467-020-19684-y
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Funding
- European Union [101003627, 733176]
- BMGF [INV-00636]
- FWO Flanders [30981113]
- FWO Hercules Foundation
- KU Leuven Rega Foundation, Internal Funds KU Leuven [3M170314]
- Stichting Antoine Faes
- China Scholarship Council (CSC)
- doctoral grant from HONOURs Marie-Sklodowska-Curie training network [721367]
- FWO Flanders SB grant [1S28617N]
- FWO [1001719N]
- KU Leuven Internal Funds [C24/17/061, C3/19/057, C16/17/010]
- FWO SB grant [1S28617N]
- Ghent University GOA
- VIB, UGent
- FWO emergency Covid-19 grants
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Emergence of SARS-CoV-2 causing COVID-19 has resulted in hundreds of thousands of deaths. In search for key targets of effective therapeutics, robust animal models mimicking COVID-19 in humans are urgently needed. Here, we show that Syrian hamsters, in contrast to mice, are highly permissive to SARS-CoV-2 and develop bronchopneumonia and strong inflammatory responses in the lungs with neutrophil infiltration and edema, further confirmed as consolidations visualized by micro-CT alike in clinical practice. Moreover, we identify an exuberant innate immune response as key player in pathogenesis, in which STAT2 signaling plays a dual role, driving severe lung injury on the one hand, yet restricting systemic virus dissemination on the other. Our results reveal the importance of STAT2-dependent interferon responses in the pathogenesis and virus control during SARS-CoV-2 infection and may help rationalizing new strategies for the treatment of COVID-19 patients. SARS-CoV-2 infection can result in severe lung inflammation and pathology, but host response remains incompletely understood. Here the authors show in Syrian hamsters that STAT2 signaling restricts systemic virus dissemination but also drives severe lung injury, playing a dual role in SARS-CoV-2 infection.
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