ArticlemBio2022
Characterization of SARS-CoV-2 Variants B.1.617.1 (Kappa), B.1.617.2 (Delta), and B.1.618 by Cell Entry and Immune Evasion.
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.
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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, 35 citations in OpenAlex.
- Leveraging knowledge graphs and large language models for integrating molecular variants and clinical insights in COVID-19 research.Biosafety and health · 2026Article
- Molecular mechanisms of SARS-CoV-2 entry: implications for biomedical strategies.Microbiology and molecular biology reviews : MMBR · 2025Review
- Early 2022 breakthrough infection sera from India target the conserved cryptic class 5 epitope to counteract immune escape by SARS-CoV-2 variants.Journal of virology · 2025Article
- Differential Impact of Spike Protein Mutations on SARS-CoV-2 Infectivity and Immune Evasion: Insights from Delta and Kappa Variants.Journal of microbiology and biotechnology · 2024Article
- Jamaican fruit bat (Artibeus jamaicensis) insusceptibility to mucosal inoculation with SARS-CoV-2 Delta variant is not caused by receptor compatibility.Npj viruses · 2024Article
- Establishment of replication-competent vesicular stomatitis virus recapitulating SADS-CoV entry.Journal of virology · 2024Article
- Single-molecule force stability of the SARS-CoV-2-ACE2 interface in variants-of-concern.Nature nanotechnology · 2024Article
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- A SARS-CoV-2: Companion Animal Transmission and Variants Classification.Pathogens (Basel, Switzerland) · 2023Review
- Spike substitution T813S increases Sarbecovirus fusogenicity by enhancing the usage of TMPRSS2.PLoS pathogens · 2023Article
- Evolution of Immune Evasion and Host Range Expansion by the SARS-CoV-2 B.1.1.529 (Omicron) Variant.mBio · 2023Article
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- A perspective on SARS-CoV-2 virus-like particles vaccines.International immunopharmacology · 2023Review
- S Trimer Derived from SARS-CoV-2 B.1.351 and B.1.618 Induced Effective Immune Response against Multiple SARS-CoV-2 Variants.Vaccines · 2023Article
- Inducing enhanced neutralizing antibodies against broad SARS-CoV-2 variants through glycan-shielding multiple non-neutralizing epitopes of RBD.Frontiers in immunology · 2023Article
- Key mutations in the spike protein of SARS-CoV-2 affecting neutralization resistance and viral internalization.Journal of medical virology · 2023Article
- Spike mutations contributing to the altered entry preference of SARS-CoV-2 omicron BA.1 and BA.2.Emerging microbes & infections · 2022Article
- Development of a simple genotyping method based on indel mutations to rapidly screen SARS-CoV-2 circulating variants: Delta, Omicron BA.1 and BA.2.Journal of virological methods · 2022Article
- The Alpha Variant (B.1.1.7) of SARS-CoV-2 Failed to Become Dominant in Mexico.Microbiology spectrum · 2022Article
Corrections and comments
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Authors and funding
16 authors at 6 institutions in 2 countries.
Funding
Abstract
Recently, highly transmissible severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants B.1.617.1 (Kappa), B.1.617.2 (Delta), and B.1.618 with mutations within the spike proteins were identified in India. The spike protein of Kappa contains the four mutations E154K, L452R, E484Q, and P681R, and Delta contains L452R, T478K, and P681R, while B.1.618 spike harbors mutations Δ145-146 and E484K. However, it remains unknown whether these variants have alterations in their entry efficiency, host tropism, and sensitivity to neutralizing antibodies as well as entry inhibitors. In this study, we found that Kappa, Delta, or B.1.618 spike uses human angiotensin-converting enzyme 2 (ACE2) with no or slightly increased efficiency, while it gains a significantly increased binding affinity with mouse, marmoset, and koala ACE2 orthologs, which exhibit limited binding with wild-type (WT) spike. Furthermore, the P681R mutation leads to enhanced spike cleavage, which could facilitate viral entry. In addition, Kappa, Delta, and B.1.618 exhibit a reduced sensitivity to neutralization by convalescent-phase sera due to the mutation E484Q, T478K, Δ145-146, or E484K, but remain sensitive to entry inhibitors such as ACE2-Ig decoy receptor. Collectively, our study revealed that enhanced human and mouse ACE2 receptor engagement, increased spike cleavage, and reduced sensitivity to neutralization antibodies of Kappa, Delta and B.1.618 may contribute to the rapid spread of these variants. Furthermore, our results also highlight that ACE2-Ig could be developed as a broad-spectrum antiviral strategy against SARS-CoV-2 variants.
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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.