Evidence map›Paper›PMID 37443189›Full record

ArticleNature ecology & evolution2023

Immune evasion and ACE2 binding affinity contribute to SARS-CoV-2 evolution.

Wentai Ma, Haoyi Fu, Fanchong Jian, Yunlong Cao, Mingkun Li

Abstract read
PubMed Publisher
In one paragraph

Article in Nature ecology & evolution, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
14.0field-weighted citation impact, top 1% 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

45 citing papers in PubMed, 72 citations in OpenAlex.

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  15. Molecular mechanisms of RaTG13 and SARS-CoV-2 RBD bound to Rhinolophus affinis bat ACE2.Protein science : a publication of the Protein Society · 2025
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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

5 authors at 3 institutions in 1 country.

Wentai MaBeijing Institute of Genomics, Chinese Academy of Sciences, and China National Center for Bioinformation, Beijing, China.ORCID http://orcid.org/0000-0003-1931-8687
Haoyi FuBeijing Institute of Genomics, Chinese Academy of Sciences, and China National Center for Bioinformation, Beijing, China.
Fanchong JianBiomedical Pioneering Innovation Center (BIOPIC), Peking University, Beijing, China.ORCID http://orcid.org/0000-0001-8703-3507
Yunlong CaoBiomedical Pioneering Innovation Center (BIOPIC), Peking University, Beijing, China. yunlongcao@pku.edu.cn.ORCID http://orcid.org/0000-0001-5918-1078
Mingkun LiBeijing Institute of Genomics, Chinese Academy of Sciences, and China National Center for Bioinformation, Beijing, China. limk@big.ac.cn.ORCID http://orcid.org/0000-0003-1041-1172
Chinese Academy of Sciences · CNPeking University · CNBeijing Institute of Genomics · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutations in the SARS-CoV-2 genome could confer resistance to pre-existing antibodies and/or increased transmissibility. The recently emerged Omicron subvariants exhibit a strong tendency for immune evasion, suggesting adaptive evolution. However, because previous studies have been limited to specific lineages or subsets of mutations, the overall evolutionary trajectory of SARS-CoV-2 and the underlying driving forces are still not fully understood. Here we analysed all open-access SARS-CoV-2 genomes (up to November 2022) and correlated the mutation incidence and fitness changes with the impacts of mutations on immune evasion and ACE2 binding affinity. Our results show that the Omicron lineage had an accelerated mutation rate in the RBD region, while the mutation incidence in other genomic regions did not change dramatically over time. Mutations in the RBD region exhibited a lineage-specific pattern and tended to become more aggregated over time, and the mutation incidence was positively correlated with the strength of antibody pressure. Additionally, mutation incidence was positively correlated with changes in ACE2 binding affinity, but with a lower correlation coefficient than with immune evasion. In contrast, the effect of mutations on fitness was more closely correlated with changes in ACE2 binding affinity than with immune evasion. Our findings suggest that immune evasion and ACE2 binding affinity play significant and diverse roles in the evolution of SARS-CoV-2.

Indexed as

COVID-19Immune EvasionAngiotensin-Converting Enzyme 2HumansMutationSARS-CoV-2ACE2 protein, humanAngiotensin-Converting Enzyme 2

Identifiers

PMID37443189
OpenAlexW4384206834

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.