ArticlePLoS pathogens2021
ACE2-lentiviral transduction enables mouse SARS-CoV-2 infection and mapping of receptor interactions.
Article in PLoS pathogens, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 47 citations in OpenAlex.
- Comparative systemic pathogenicity and host tropism of ancestral SARS-CoV-2, Delta, and Omicron EG.5 variants in K18-hACE2 mice.Frontiers in immunology · 2026Article
- Experimental evolution of Rc-o319 sarbecovirus spike protein reveals limited ACE2 adaptability.Virus evolution · 2026Article
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- Scar wars: the viral menace.American journal of physiology. Lung cellular and molecular physiology · 2025Review
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- Determinants of susceptibility to SARS-CoV-2 infection in murine ACE2.Journal of virology · 2025Article
- Marginal cytokine modulation by Schistosoma mansoni soluble egg antigen in SARS-CoV-2-infected K18-hACE2 mice.Folia parasitologica · 2025Article
- SARS-CoV-2 spike protein induces salivary gland dysfunction and immune infiltration in C57BL/6 mice.Frontiers in immunology · 2025Article
- Evolution of Zika virus inVirus evolution · 2025Article
- FDA-approved drug repurposing screen identifies inhibitors of SARS-CoV-2 pseudovirus entry.Frontiers in pharmacology · 2025Article
- Article
- SARS-CoV-2 immunity in animal models.Cellular & molecular immunology · 2024Review
- Adaptation of SARS-CoV-2 to ACE2Journal of virology · 2024Article
- Tracking inflammation resolution signatures in lungs after SARS-CoV-2 omicron BA.1 infection of K18-hACE2 mice.PloS one · 2024Article
- The effects of iron deficient and high iron diets on SARS-CoV-2 lung infection and disease.Frontiers in microbiology · 2024Article
- CCR5/CXCR3 antagonist TAK-779 prevents diffuse alveolar damage of the lung in the murine model of the acute respiratory distress syndrome.Frontiers in pharmacology · 2024Article
- The Y498T499-SARS-CoV-2 spike (S) protein interacts poorly with rat ACE2 and does not affect the rat lung.Access microbiology · 2024Article
- Microplastics dysregulate innate immunity in the SARS-CoV-2 infected lung.Frontiers in immunology · 2024Article
- Investigation of SARS-CoV-2 individual proteins reveals the in vitro and in vivo immunogenicity of membrane protein.Scientific reports · 2023Article
- Comparative Efficacy of Mayaro Virus-Like Particle Vaccines Produced in Insect or Mammalian Cells.Journal of virology · 2023Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SARS-CoV-2 uses the human ACE2 (hACE2) receptor for cell attachment and entry, with mouse ACE2 (mACE2) unable to support infection. Herein we describe an ACE2-lentivirus system and illustrate its utility for in vitro and in vivo SARS-CoV-2 infection models. Transduction of non-permissive cell lines with hACE2 imparted replication competence, and transduction with mACE2 containing N30D, N31K, F83Y and H353K substitutions, to match hACE2, rescued SARS-CoV-2 replication. Intrapulmonary hACE2-lentivirus transduction of C57BL/6J mice permitted significant virus replication in lung epithelium. RNA-Seq and histological analyses illustrated that this model involved an acute inflammatory disease followed by resolution and tissue repair, with a transcriptomic profile similar to that seen in COVID-19 patients. hACE2-lentivirus transduction of IFNAR-/- and IL-28RA-/- mouse lungs was used to illustrate that loss of type I or III interferon responses have no significant effect on virus replication. However, their importance in driving inflammatory responses was illustrated by RNA-Seq analyses. We also demonstrate the utility of the hACE2-lentivirus transduction system for vaccine evaluation in C57BL/6J mice. The ACE2-lentivirus system thus has broad application in SARS-CoV-2 research, providing a tool for both mutagenesis studies and mouse model development.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.