ArticlemBio2022
Evidence for an ACE2-Independent Entry Pathway That Can Protect from Neutralization by an Antibody Used for COVID-19 Therapy.
Article in mBio, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- Human keratinocytes exhibit limited potential for SARS-CoV-2 infection despite ACE2 and mature cathepsin L expression.JID innovations : skin science from molecules to population health · 2026Article
- Review
- Convergent Evolution and Host-Limiting Impacts of SARS-CoV-2 Revealed by Cellular Experiments.Molecular biology and evolution · 2025Article
- Patterns of Recombination in Coronaviruses.International journal of molecular sciences · 2025Article
- Host cell lectins ASGR1 and DC-SIGN jointly with TMEM106B confer ACE2 independence and imdevimab resistance to SARS-CoV-2 pseudovirus with spike mutation E484D.Journal of virology · 2025Article
- Spike substitutions E484D, P812R and Q954H mediate ACE2-independent entry of SARS-CoV-2 across different cell lines.PloS one · 2025Article
- Neutralisation resistance of SARS-CoV-2 spike-variants is primarily mediated by synergistic receptor binding domain substitutions.Emerging microbes & infections · 2024Article
- ACE2-independent sarbecovirus cell entry can be supported by TMPRSS2-related enzymes and can reduce sensitivity to antibody-mediated neutralization.PLoS pathogens · 2024Article
- A basally active cGAS-STING pathway limits SARS-CoV-2 replication in a subset of ACE2 positive airway cell models.Nature communications · 2024Article
- A basally active cGAS-STING pathway limits SARS-CoV-2 replication in a subset of ACE2 positive airway cell models.bioRxiv : the preprint server for biology · 2024Article
- The TRAF3-DYRK1A-RAD54L2 complex maintains ACE2 expression to promote SARS-CoV-2 infection.Journal of virology · 2024Article
- Cell type-specific adaptation of the SARS-CoV-2 spike.Virus evolution · 2024Article
- Structural basis of white-tailed deer,Journal of virology · 2023Article
- ACE2-EGFR-MAPK signaling contributes to SARS-CoV-2 infection.Life science alliance · 2023Article
- Article
- Testicular pathological alterations associated with SARS-CoV-2 infection.Frontiers in reproductive health · 2023Review
- Identification of a pharmacological approach to reduce ACE2 expression and development of anJournal of virus eradication · 2022Article
- ACE2-Independent Alternative Receptors for SARS-CoV-2.Viruses · 2022Review
- Host Cell Entry and Neutralization Sensitivity of SARS-CoV-2 Lineages B.1.620 and R.1.Viruses · 2022Article
- Senescent endothelial cells are predisposed to SARS-CoV-2 infection and subsequent endothelial dysfunction.Scientific reports · 2022Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SARS-CoV-2 variants of concern (VOC) acquired mutations in the spike (S) protein, including E484K, that confer resistance to neutralizing antibodies. However, it is incompletely understood how these mutations impact viral entry into host cells. Here, we analyzed how mutations at position 484 that have been detected in COVID-19 patients impact cell entry and antibody-mediated neutralization. We report that mutation E484D markedly increased SARS-CoV-2 S-driven entry into the hepatoma cell line Huh-7 and the lung cell NCI-H1299 without augmenting ACE2 binding. Notably, mutation E484D largely rescued Huh-7 but not Vero cell entry from blockade by the neutralizing antibody Imdevimab and rendered Huh-7 cell entry ACE2-independent. These results suggest that the naturally occurring mutation E484D allows SARS-CoV-2 to employ an ACE2-independent mechanism for entry that is largely insensitive against Imdevimab, an antibody employed for COVID-19 therapy.
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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.