Evidence map›Paper›PMID 40811064›Full record

ArticleCell reports2025

Signatures of omicron-like adaptation in early SARS-CoV-2 variants and chronic infection.

Mark Tsz Kin Cheng, Mazharul Altaf, Jesu Castin, Ann-Kathrin Reuschl, Benjamin L Sievers, Kimia Kamelian, Dejan Mesner, Rebecca B Morse, Adam Abdullahi, Bo Meng and 8 more

Abstract read
In one paragraph

Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Mycophenolic acid treatment drives the emergence of novel SARS-CoV-2 variants.Proceedings of the National Academy of Sciences of the United States of America · 2025
    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

18 authors.

Mark Tsz Kin ChengDepartment of Medicine, University of Cambridge, Cambridge, UK; Cambridge Institute of Therapeutic Immunology & Infectious Disease (CITIID), Cambridge, UK.
Mazharul AltafDepartment of Medicine, University of Cambridge, Cambridge, UK; Cambridge Institute of Therapeutic Immunology & Infectious Disease (CITIID), Cambridge, UK.
Jesu CastinCSIR-Institute of Genomics and Integrative Biology, Mathura Road, New Delhi 110025, India; Academy of Scientific and Innovative Research (AcSIR), Ghaziabad 201002, India.
Ann-Kathrin ReuschlDivision of Infection and Immunity, University College London, London, UK.
Benjamin L SieversDepartment of Medicine, University of Cambridge, Cambridge, UK; Cambridge Institute of Therapeutic Immunology & Infectious Disease (CITIID), Cambridge, UK.
Kimia KamelianDepartment of Medicine, University of Cambridge, Cambridge, UK; Cambridge Institute of Therapeutic Immunology & Infectious Disease (CITIID), Cambridge, UK.
Dejan MesnerDivision of Infection and Immunity, University College London, London, UK.
Rebecca B MorseDepartment of Medicine, University of Cambridge, Cambridge, UK; Cambridge Institute of Therapeutic Immunology & Infectious Disease (CITIID), Cambridge, UK.
Adam AbdullahiDepartment of Medicine, University of Cambridge, Cambridge, UK; Cambridge Institute of Therapeutic Immunology & Infectious Disease (CITIID), Cambridge, UK.
Bo MengDepartment of Medicine, University of Cambridge, Cambridge, UK; Cambridge Institute of Therapeutic Immunology & Infectious Disease (CITIID), Cambridge, UK.
Kata CsibaDepartment of Medicine, University of Cambridge, Cambridge, UK; Cambridge Institute of Therapeutic Immunology & Infectious Disease (CITIID), Cambridge, UK.
Cambridge NIHR Bioresource
Steven A KempDepartment of Medicine, University of Cambridge, Cambridge, UK; Cambridge Institute of Therapeutic Immunology & Infectious Disease (CITIID), Cambridge, UK.
Darren P MartinDivision of Computational Biology, Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Cape Town 7700, South Africa.
Clare JollyDivision of Infection and Immunity, University College London, London, UK.
Christopher RuisDivision of Infection and Immunity, University College London, London, UK; Victor Philip Dahdaleh Heart & Lung Research Institute, University of Cambridge, Cambridge, UK; Cambridge Centre for AI in Medicine, University of Cambridge, Cambridge, UK; Department of Veterinary Medicine, University of Cambridge, Cambridge, UK.
Lipi ThukralCSIR-Institute of Genomics and Integrative Biology, Mathura Road, New Delhi 110025, India; Academy of Scientific and Innovative Research (AcSIR), Ghaziabad 201002, India. Electronic address: lipi.thukral@igib.res.in.
Ravindra K GuptaDepartment of Medicine, University of Cambridge, Cambridge, UK; Cambridge Institute of Therapeutic Immunology & Infectious Disease (CITIID), Cambridge, UK; Africa Health Research Institute, Durban, KZN, South Africa; Hong Kong Jockey Club Global Health Institute, Hong Kong, China. Electronic address: rkg20@cam.ac.uk.

Funding

Wellcome Trust 223065
6 · The paper itself

Abstract

Persistent severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections are a source of new variants and can provide insight into evolutionary trajectories. Here, we observe upper airway-specific evolution of SARS-CoV-2, demonstrating a fusion peptide (FP) domain mutation (S:P812S) adjacent to the S2' cleavage site that emerged during a chronic infection. Indeed, this mutation had emerged previously and been transmitted in a delta variant lineage. P812S in a spike-pseudotyped virus did not impact entry efficiency. However, cleavage at S1/S2 was reduced, and molecular dynamics simulation demonstrated altered S1/S2 loop conformations. Consistent with impaired S1/S2 cleavage, and reminiscent of Omicron BA.1, cell-cell fusogenicity was severely impaired by P812S. P812S conferred evasion of a FP-targeting monoclonal antibody, consistent with FP-region structural rearrangements. Finally, P812S-bearing viruses showed evasion of polyclonal neutralizing antibodies in sera from vaccinated individuals at 32C. These data shed light on the balance between SARS-CoV-2 upper airway adaptation/immune evasion, syncytium formation, and pathogenic potential.

Indexed as

COVID-19SARS-CoV-2AnimalsAntibodies, NeutralizingAntibodies, ViralChronic DiseaseHumansImmune EvasionMolecular Dynamics SimulationMutationSpike Glycoprotein, CoronavirusVirus InternalizationAntibodies, NeutralizingAntibodies, ViralSpike Glycoprotein, Coronavirusspike protein, SARS-CoV-2COVID-19CP: MicrobiologyevolutionfusionimmunocompromisedinfectivityomicronSARS CoV-2serology

Identifiers

PMID40811064
PMCPMC7618492

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.