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Robertson, Shelly J; Bedard, Olivia; McNally, Kristin L; Shaia, Carl; Clancy, Chad S; Lewis, Matthew; Broeckel, Rebecca M; Chiramel, Abhilash I; Shannon, Jeffrey G; Sturdevant, Gail L; Rosenke, Rebecca; Anzick, Sarah L; Forte, Elvira; Preuss, Christoph; Baker, Candice N; Harder, Jeffrey M; Brunton, Catherine; Munger, Steven; Bruno, Daniel P; Lack, Justin B; Leung, Jacqueline M; Shamsaddini, Amirhossein; Gardina, Paul; Sturdevant, Daniel E; Sun, Jian; Martens, Craig; Holland, Steven M; Rosenthal, Nadia A; Best, Sonja M
Nature communications, 07/2023, Letnik: 14, Številka: 1Journal Article
Inflammation in response to severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection drives severity of coronavirus disease 2019 (COVID-19) and is influenced by host genetics. To understand mechanisms of inflammation, animal models that reflect genetic diversity and clinical outcomes observed in humans are needed. We report a mouse panel comprising the genetically diverse Collaborative Cross (CC) founder strains crossed to human ACE2 transgenic mice (K18-hACE2) that confers susceptibility to SARS-CoV-2. Infection of CC x K18-hACE2 resulted in a spectrum of survival, viral replication kinetics, and immune profiles. Importantly, in contrast to the K18-hACE2 model, early type I interferon (IFN-I) and regulated proinflammatory responses were required for control of SARS-CoV-2 replication in PWK x K18-hACE2 mice that were highly resistant to disease. Thus, virus dynamics and inflammation observed in COVID-19 can be modeled in diverse mouse strains that provide a genetically tractable platform for understanding anti-coronavirus immunity.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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Vir: Osebne bibliografije
in: SICRIS
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