Evidence map›Paper›PMID 40333265›Full record

ArticleVaccines2025

Entry Efficiency, Protease Dependence, and Antibody-Mediated Neutralization of SARS-CoV-2 Sublineages KP.3.1.1 and XEC.

Prerna Arora, Amy Kempf, Inga Nehlmeier, Sebastian R Schulz, Hans-Martin Jäck, Markus Hoffmann, Stefan Pöhlmann

Abstract read
In one paragraph

Article in Vaccines, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Prerna AroraInfection Biology Unit, German Primate Center-Leibniz Institute for Primate Research, 37077 Göttingen, Germany.ORCID 0000-0002-0618-8652
Amy KempfInfection Biology Unit, German Primate Center-Leibniz Institute for Primate Research, 37077 Göttingen, Germany.
Inga NehlmeierInfection Biology Unit, German Primate Center-Leibniz Institute for Primate Research, 37077 Göttingen, Germany.
Sebastian R SchulzDivision of Molecular Immunology, Department of Internal Medicine 3, Friedrich-Alexander University of Erlangen-Nürnberg, 91054 Erlangen, Germany.
Hans-Martin JäckDivision of Molecular Immunology, Department of Internal Medicine 3, Friedrich-Alexander University of Erlangen-Nürnberg, 91054 Erlangen, Germany.ORCID 0000-0002-6332-8463
Markus HoffmannInfection Biology Unit, German Primate Center-Leibniz Institute for Primate Research, 37077 Göttingen, Germany.ORCID 0000-0003-4603-7696
Stefan PöhlmannInfection Biology Unit, German Primate Center-Leibniz Institute for Primate Research, 37077 Göttingen, Germany.ORCID 0000-0001-6086-9136

Funding

Bavarian State Ministry for Science and the Arts and Deutsche Forschungsgemeinschaft RTG1660 and TRR130BMBF 01KI2043, NaFoUniMedCovid19-COVIM: 01KX2021EU project UNDINE 101057100Ministry of Science and Culture of Lower Saxony in Germany 14-76103-184 and 14-76403-184, projects 7FF22, 6FF22, 10FF22
6 · The paper itself

Abstract

backgroundThe SARS-CoV-2 variants KP.3.1.1 and XEC currently dominate the COVID-19 epidemic. However, their cell tropism, proteolytic processing, and susceptibility to neutralization by monoclonal antibodies remain incompletely characterized.

methodsWe employed pseudotyped viruses to assess the entry efficiency of KP.3.1.1 and XEC in various cell lines, their dependence on TMPRSS2 for lung cell entry, and their ability to use ACE2 for infection. Additionally, we evaluated their susceptibility to neutralization by monoclonal antibodies BD55-4637 and BD55-5514.

resultsKP.3.1.1 and XEC entered cell lines with similar efficiency as the parental JN.1 lineage and utilized TMPRSS2 for Calu-3 lung cell entry. Unlike JN.1, KP.3.1.1 and XEC failed to efficiently use murine ACE2 for cell entry. Both variants were effectively neutralized by the monoclonal antibodies BD55-4637 and BD55-5514, suggesting therapeutic potential.

conclusionsOur findings demonstrate that JN.1, KP.3.1.1, and XEC, like their predecessor BA.2.86, rely on TMPRSS2 for lung cell entry and remain sensitive to certain neutralizing monoclonal antibodies. However, these variants differ in their ability to utilize ACE2 species orthologs for cell entry.

Indexed as

BA.2.86 descendantscell tropismmonoclonal antibody susceptibilitySARS-CoV-2 variants

Identifiers

PMID40333265
PMCPMC12030816

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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.