{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yan K"],"funding":["QIMR Berghofer Medical Research Institute","Clive Berghofer","National Health and Medical Research Council (NHMRC) of Australia","Brazil Family Foundation"],"pagination":["veac063"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9338707"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["8(2)"],"pubmed_abstract":["Human <i>ACE2</i> Human angiotensin converting enzyme 2 (hACE2) is the key cell attachment and entry receptor for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), with the original SARS-CoV-2 isolates unable to use mouse <i>ACE2</i> (mACE2). Herein we describe the emergence of a SARS-CoV-2 strain capable of <i>ACE2</i>-independent infection and the evolution of mouse-adapted (MA) SARS-CoV-2 by <i>in vitro</i> serial passaging of virus in co-cultures of cell lines expressing hACE2 and mACE2. MA viruses evolved with up to five amino acid changes in the spike protein, all of which have been seen in human isolates. MA viruses replicated to high titers in C57BL/6J mouse lungs and nasal turbinates and caused characteristic lung histopathology. One MA virus also evolved to replicate "],"journal":["Virus evolution"],"pubmed_title":["Evolution of ACE2-independent SARS-CoV-2 infection and mouse adaption after passage in cells expressing human and mouse ACE2."],"pmcid":["PMC9338707"],"funding_grant_id":["Intramural seed grant","APP1173880","Philanthropic"],"pubmed_authors":["Yan K","Bishop CR","Suhrbier A","Rawle DJ","Tang B","Le TT","Dumenil T"],"additional_accession":[]},"is_claimable":false,"name":"Evolution of ACE2-independent SARS-CoV-2 infection and mouse adaption after passage in cells expressing human and mouse ACE2.","description":"Human <i>ACE2</i> Human angiotensin converting enzyme 2 (hACE2) is the key cell attachment and entry receptor for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), with the original SARS-CoV-2 isolates unable to use mouse <i>ACE2</i> (mACE2). Herein we describe the emergence of a SARS-CoV-2 strain capable of <i>ACE2</i>-independent infection and the evolution of mouse-adapted (MA) SARS-CoV-2 by <i>in vitro</i> serial passaging of virus in co-cultures of cell lines expressing hACE2 and mACE2. MA viruses evolved with up to five amino acid changes in the spike protein, all of which have been seen in human isolates. MA viruses replicated to high titers in C57BL/6J mouse lungs and nasal turbinates and caused characteristic lung histopathology. One MA virus also evolved to replicate ","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022","modification":"2026-06-18T03:16:21.834Z","creation":"2025-02-19T03:29:22.777Z"},"accession":"S-EPMC9338707","cross_references":{"pubmed":["35919871"],"doi":["10.1093/ve/veac063"]}}