Evidence map›Paper›PMID 40272156›Full record

ArticleJournal of virology2025

SARS-CoV-2 biological clones are genetically heterogeneous and include clade-discordant residues.

Ana Isabel de Ávila, María Eugenia Soria, Brenda Martínez-González, Pilar Somovilla, Pablo Mínguez, Llanos Salar-Vidal, Mario Esteban-Muñoz, Marta Martín-García, Sonia Zuñiga, Isabel Sola and 4 more

Abstract read
In one paragraph

Article in Journal of virology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. SARS-CoV-2 mutant spectrum complexity is an epidemiologically evolvable trait.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

14 authors.

Ana Isabel de ÁvilaCentro de Biología Molecular "Severo Ochoa" (CSIC-UAM), Campus de Cantoblanco, Madrid, Spain.ORCID 0000-0002-9381-0963
María Eugenia SoriaCentro de Biología Molecular "Severo Ochoa" (CSIC-UAM), Campus de Cantoblanco, Madrid, Spain.ORCID 0000-0002-4719-3351
Brenda Martínez-GonzálezDepartment of Clinical Microbiology, Instituto de Investigación Sanitaria-Fundación Jiménez Díaz University Hospital, Universidad Autónoma de Madrid (IIS-FJD, UAM), Madrid, Spain.
Pilar SomovillaCentro de Biología Molecular "Severo Ochoa" (CSIC-UAM), Campus de Cantoblanco, Madrid, Spain.ORCID 0000-0001-8368-3641
Pablo MínguezDepartment of Genetics and Genomics, Instituto de Investigación Sanitaria-Fundación Jiménez Díaz University Hospital, Universidad Autónoma de Madrid (IIS-FJD, UAM), Madrid, Spain.ORCID 0000-0003-4099-9421
Llanos Salar-VidalDepartment of Clinical Microbiology, Instituto de Investigación Sanitaria-Fundación Jiménez Díaz University Hospital, Universidad Autónoma de Madrid (IIS-FJD, UAM), Madrid, Spain.ORCID 0000-0002-3052-0176
Mario Esteban-MuñozDepartment of Clinical Microbiology, Instituto de Investigación Sanitaria-Fundación Jiménez Díaz University Hospital, Universidad Autónoma de Madrid (IIS-FJD, UAM), Madrid, Spain.
Marta Martín-GarcíaDepartment of Clinical Microbiology, Instituto de Investigación Sanitaria-Fundación Jiménez Díaz University Hospital, Universidad Autónoma de Madrid (IIS-FJD, UAM), Madrid, Spain.ORCID 0009-0003-9724-4422
Sonia ZuñigaDepartment of Molecular and Cell Biology, Centro Nacional de Biotecnología (CNB-CSIC), Consejo Superior de Investigaciones Científicas (CSIC), Campus de Cantoblanco, Madrid, Spain.ORCID 0000-0003-2549-6826
Isabel SolaDepartment of Molecular and Cell Biology, Centro Nacional de Biotecnología (CNB-CSIC), Consejo Superior de Investigaciones Científicas (CSIC), Campus de Cantoblanco, Madrid, Spain.ORCID 0000-0002-5704-1917
Luis EnjuanesDepartment of Molecular and Cell Biology, Centro Nacional de Biotecnología (CNB-CSIC), Consejo Superior de Investigaciones Científicas (CSIC), Campus de Cantoblanco, Madrid, Spain.ORCID 0000-0002-0854-0226
Ignacio GadeaDepartment of Clinical Microbiology, Instituto de Investigación Sanitaria-Fundación Jiménez Díaz University Hospital, Universidad Autónoma de Madrid (IIS-FJD, UAM), Madrid, Spain.ORCID 0000-0003-4684-7816
Celia PeralesDepartment of Clinical Microbiology, Instituto de Investigación Sanitaria-Fundación Jiménez Díaz University Hospital, Universidad Autónoma de Madrid (IIS-FJD, UAM), Madrid, Spain.ORCID 0000-0003-1618-1937
Esteban DomingoCentro de Biología Molecular "Severo Ochoa" (CSIC-UAM), Campus de Cantoblanco, Madrid, Spain.ORCID 0000-0002-0573-1676

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Defective genomes are part of SARS-CoV-2 quasispecies. High-resolution, ultra-deep sequencing of bulk RNA from viral populations does not distinguish RNA mutations, insertions, and deletions in viable genomes from those in defective genomes. To quantify SARS-CoV-2 infectious variant progeny, virus from four individual plaques (biological clones) of a preparation of isolate USA-WA1/2020, formed on Vero E6 cell monolayers, was subjected to further biological cloning to yield 9 second-generation and 15 third-generation sub-clones. Consensus genomic sequences of the biological clones and sub-clones included an average of 2.8 variations per viable genome, relative to the consensus sequence of the parental USA-WA1/2020 virus. This value is 6.5-fold lower than the estimates for biological clones of other RNA viruses such as bacteriophage Qβ, foot-and-mouth disease virus, or hepatitis C virus in cell culture. The mutant spectrum complexity of the nsp12 (polymerase)- and spike (S)-coding region was unique in the progeny of each of 10 third-generation sub-clones; they shared 2.4% of the total of 164 different mutations and deletions scored in the 3,719 genomic residues that were screened. The presence of minority out-of-frame deletions revealed the ease of defective genome production from an individual infectious genome. Several low-frequency point mutations and deletions were clade-discordant in that they were not typical of USA-WA1/2020 but served to define the consensus sequences of future SARS-CoV-2 clades. Implications for SARS-CoV-2 adaptability and COVID-19 control of the viable genome heterogeneity and the generation of complex mutant spectra from individual genomes are discussed.IMPORTANCESequencing of biological clones is a means to identify mutations, insertions, and deletions located in viable genomes. This distinction is particularly important for viral populations, such as those of SARS-CoV-2, that contain large proportions of defective genomes. By sequencing biological clones and sub-clones, we quantified the heterogeneity of the viable complement of USA-WA1/2020 to be lower than exhibited by other RNA viruses. This difference may be due to a reduced mutation rate or to limited tolerance of the large coronavirus genome to incorporate mutations and deletions and remain functional or a combination of both influences. The presence of clade-discordant residues in the progeny of individual biological sub-clones suggests limitations in the occupation of sequence space by SARS-CoV-2. However, the complex and unique mutant spectra that are rapidly generated from individual genomes suggest an aptness to confront selective constraints.

Indexed as

SARS-CoV-2AnimalsChlorocebus aethiopsCOVID-19Genome, ViralHumansMutationRNA, ViralSpike Glycoprotein, CoronavirusVero CellsRNA, ViralSpike Glycoprotein, Coronavirusspike protein, SARS-CoV-2defective viral genomedeletiondiversity indicesmutant spectrumpoint mutationpopulation complexityquasispeciesRNA virusultra-deep sequencingviral clade

Identifiers

PMID40272156
PMCPMC12090815

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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.