uww9aa3

Property	Value
?:abstract	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.
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?:doi	10.1038/s41467-020-19684-y
?:doi	<https://research.tib.eu/covid-19/entity/10.1038/s41467-020-19684-y>
?:journal	Nat_Commun
?:license	cc-by
?:pdf_json_files	document_parses/pdf_json/9abb259c8ea4cfacdc9b879b5fd5bf1e19d4eaf1.json; document_parses/pdf_json/66b64a576ae53cd001bccbbb947bfac1e8ebc951.json
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?:pmid	<https://research.tib.eu/covid-19/entity/33203860.0>
?:pmid	33203860.0
?:publication_isRelatedTo_Disease	<https://research.tib.eu/covid-19/entity/COVID-19>
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?:source	Medline; PMC
?:title	STAT2 signaling restricts viral dissemination but drives severe pneumonia in SARS-CoV-2 infected hamsters
?:type	<https://research.tib.eu/covid-19/vocab/Publication>
?:year	2020-11-17

Property

Value

?:abstract

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.

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