Evidence map›Paper›PMID 34997962›Full record

ArticleJournal of medical virology2022

The puzzling mutational landscape of the SARS-2-variant Omicron.

Jacques Fantini, Nouara Yahi, Philippe Colson, Henri Chahinian, Bernard La Scola, Didier Raoult

Open access · greenAbstract read
In one paragraph

Article in Journal of medical virology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
8.2field-weighted citation impact, top 2% of its field
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

48 citing papers in PubMed, 83 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Jacques FantiniDepartment of Biology, Aix-Marseille Université, Marseille, France.ORCID http://orcid.org/0000-0001-8653-5521
Nouara YahiDepartment of Biology, Aix-Marseille Université, Marseille, France.
Philippe ColsonDepartment of Biology, Aix-Marseille Université, Marseille, France.ORCID http://orcid.org/0000-0001-6285-0308
Henri ChahinianDepartment of Biology, Aix-Marseille Université, Marseille, France.
Bernard La ScolaDepartment of Biology, Aix-Marseille Université, Marseille, France.
Didier RaoultDepartment of Biology, Aix-Marseille Université, Marseille, France.
Aix-Marseille Université · FRInserm · FR

Funding

This work was supported by the French Government under the "Investments for the Future" program managed by the National Agency for Research (ANR), Méditerranée-Infection 10-IAHU-03 and was also supported by Région Provence Alpes Côte d'Azur and European funding FEDER PRIMMI (Fonds Européen de Développement Régional-Plateformes de Recherche et d'Innovation Mutualisées Méditerranée Infection), FEDER PA 0000320 PRIMMI, and by Hitachi High-Technologies Corporation, Tokyo, Japan.
6 · The paper itself

Abstract

The recently emerging SARS-CoV-2 variant omicron displays an unusual association of 30 mutations, 3 deletions, and 1 insertion. To analyze the impact of this atypic mutational landscape, we constructed a complete structure of the omicron spike protein. Compared with the delta variant, the receptor-binding domain (RBD) of omicron has an increased electrostatic surface potential, but a decreased affinity for the ACE-2 receptor. The N-terminal domain (NTD) has both a decreased surface potential and a lower affinity for lipid rafts. The omicron variant is predicted to be less fusogenic and thus less pathogenic than delta, due to a geometric reorganization of the S1-S2 cleavage site. Overall, these virological parameters suggest that omicron does not have a significant infectivity advantage over the delta variant. However, in omicron, neutralizing epitopes are greatly affected, suggesting that current vaccines will probably confer little protection against this variant. In conclusion, the puzzling mutational pattern of the omicron variant combines contradictory properties which may either decrease (virological properties) or increase (immunological escape/facilitation) the transmission of this variant in the human population. This Janus-like phenotype may explain some conflicting reports on the initial assessment of omicron and provide new insights about the molecular mechanisms controlling its dissemination and pathogenesis worldwide.

Indexed as

COVID-19SARS-CoV-2HumansMutationProtein Bindingantibody susceptibilitycoronavirusevolutioninfectionpathogenesisSARS coronavirusvirulencevirus classification

Identifiers

PMID34997962
PMCPMC9015223
OpenAlexW4205399263

What OpenQuestion holds

Textmetadata
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.