{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Robertson SJ"],"funding":["Intramural NIH HHS","Division of Intramural Research, National Institute of Allergy and Infectious Diseases"],"pagination":["4481"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10368652"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(1)"],"pubmed_abstract":["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 rep"],"journal":["Nature communications"],"pubmed_title":["Genetically diverse mouse models of SARS-CoV-2 infection reproduce clinical variation in type I interferon and cytokine responses in COVID-19."],"pmcid":["PMC10368652"],"funding_grant_id":["1ZIAAI001125-04","ZIA AI001125"],"pubmed_authors":["Shamsaddini A","Best SM","Bedard O","Gardina P","Harder JM","Robertson SJ","Bruno DP","Sturdevant GL","Holland SM","Leung JM","Sun J","Clancy CS","Shaia C","Chiramel AI","Brunton C","Munger S","Lewis M","Forte E","McNally KL","Broeckel RM","Preuss C","Shannon JG","Martens C","Baker CN","Rosenthal NA","Lack JB","Rosenke R","Anzick SL","Sturdevant DE"],"additional_accession":[]},"is_claimable":false,"name":"Genetically diverse mouse models of SARS-CoV-2 infection reproduce clinical variation in type I interferon and cytokine responses in COVID-19.","description":"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 rep","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jul","modification":"2025-04-04T20:33:03.812Z","creation":"2025-02-19T00:26:33.272Z"},"accession":"S-EPMC10368652","cross_references":{"pubmed":["37491352"],"doi":["10.1038/s41467-023-40076-5"]}}