ArticleeLife2022
ACE2 is the critical in vivo receptor for SARS-CoV-2 in a novel COVID-19 mouse model with TNF- and IFNγ-driven immunopathology.
Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 66 citations in OpenAlex.
- B Cell Receptor's function in virus entry: Anti-SARS-CoV-2 B cell receptors can mediate viral entry in an ACE2-independent mechanism.PLoS pathogens · 2026Article
- IFITM3 deficiency drives SARS-CoV-2 adaptation while preserving variant-specific traits.Nature communications · 2026Article
- The impact of diabetes and obesity on the severity and mortality of SARS-CoV-2 infection.Journal of diabetes and metabolic disorders · 2025Review
- Monocyte-eosinophil signaling axis promotes vaccine-mediated protection against SARS-CoV-2.PLoS pathogens · 2025Article
- Filamin A editing in myeloid cells reduces intestinal inflammation and protects from colitis.The Journal of experimental medicine · 2025Article
- The Anti-Inflammatory Potential of Levosimendan in Sepsis: An Experimental Study Using a LPS-Induced Rat Model.Life (Basel, Switzerland) · 2025Article
- ACE2, From the Kidney to SARS-CoV-2: Donald Seldin Award Lecture 2023.Hypertension (Dallas, Tex. : 1979) · 2025Article
- Prospects for the Protective Mechanisms and Compounds of Bufei Huoxue Capsule against COVID-19 Convalescence: Evaluation of Integrating UHPLC-HRMS Analysis and Network Pharmacology Strategy.Combinatorial chemistry & high throughput screening · 2025Article
- Cyclophilin-CD147 interaction enables SARS-CoV-2 infection of human monocytes and their activation via Toll-like receptors 7 and 8.Frontiers in immunology · 2025Article
- TNF-α exacerbates SARS-CoV-2 infection by stimulating CXCL1 production from macrophages.PLoS pathogens · 2024Article
- The Functions of SARS-CoV-2 Receptors in Diabetes-Related Severe COVID-19.International journal of molecular sciences · 2024Review
- Human ACE2 Gene Replacement Mice Support SARS-CoV-2 Viral Replication and Nonlethal Disease Progression.ImmunoHorizons · 2024Article
- The assembly of neutrophil inflammasomes during COVID-19 is mediated by type I interferons.PLoS pathogens · 2024Article
- IL-10 suppresses T cell expansion while promoting tissue-resident memory cell formation during SARS-CoV-2 infection in rhesus macaques.PLoS pathogens · 2024Article
- Neuropathological assessment of the olfactory bulb and tract in individuals with COVID-19.Acta neuropathologica communications · 2024Article
- Neutrophil Extracellular Traps in Cardiovascular and Aortic Disease: A Narrative Review on Molecular Mechanisms and Therapeutic Targeting.International journal of molecular sciences · 2024Review
- Altered receptor binding, antibody evasion and retention of T cell recognition by the SARS-CoV-2 XBB.1.5 spike protein.Nature communications · 2024Article
- A highly susceptible hACE2-transgenic mouse model for SARS-CoV-2 research.Frontiers in microbiology · 2024Article
- Phase I dose-escalation study to assess the safety, tolerability, pharmacokinetics and pharmacodynamics of an inhaled recombinant human ACE2.ERJ open research · 2024Article
- Differential activation of programmed cell death in patients with severe SARS-CoV-2 infection.Cell death discovery · 2023Article
Corrections and comments
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Authors and funding
24 authors at 8 institutions in 6 countries.
Funding
Abstract
Despite tremendous progress in the understanding of COVID-19, mechanistic insight into immunological, disease-driving factors remains limited. We generated maVie16, a mouse-adapted SARS-CoV-2, by serial passaging of a human isolate. In silico modeling revealed how only three Spike mutations of maVie16 enhanced interaction with murine ACE2. maVie16 induced profound pathology in BALB/c and C57BL/6 mice, and the resulting mouse COVID-19 (mCOVID-19) replicated critical aspects of human disease, including early lymphopenia, pulmonary immune cell infiltration, pneumonia, and specific adaptive immunity. Inhibition of the proinflammatory cytokines IFNγ and TNF substantially reduced immunopathology. Importantly, genetic ACE2-deficiency completely prevented mCOVID-19 development. Finally, inhalation therapy with recombinant ACE2 fully protected mice from mCOVID-19, revealing a novel and efficient treatment. Thus, we here present maVie16 as a new tool to model COVID-19 for the discovery of new therapies and show that disease severity is determined by cytokine-driven immunopathology and critically dependent on ACE2 in vivo.
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