Evidence map›Paper›PMID 39937682›Full record

ArticleeLife2025

Interleukin-1 prevents SARS-CoV-2-induced membrane fusion to restrict viral transmission via induction of actin bundles.

Xu Zheng, Shi Yu, Yanqiu Zhou, Kuai Yu, Yuhui Gao, Mengdan Chen, Dong Duan, Yunyi Li, Xiaoxian Cui, Jiabin Mou and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in eLife, 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. 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

16 authors.

Xu Zheng *The Center for Microbes, Development and Health, National Key Laboratory of Immune Response and Immunotherapy, Shanghai Institute of Immunity and Infection, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.ORCID https://orcid.org/0000-0002-1446-1882
Shi Yu *The Center for Microbes, Development and Health, National Key Laboratory of Immune Response and Immunotherapy, Shanghai Institute of Immunity and Infection, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.ORCID https://orcid.org/0000-0003-0651-4769
Yanqiu Zhou *Shanghai Municipal Center for Disease Control and Prevention, Shanghai, China.
Kuai Yu *The First Affiliated Hospital of Guangzhou Medical University, State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, Guangzhou, China.ORCID https://orcid.org/0000-0001-9699-4780
Yuhui GaoThe Center for Microbes, Development and Health, National Key Laboratory of Immune Response and Immunotherapy, Shanghai Institute of Immunity and Infection, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Mengdan ChenThe Center for Microbes, Development and Health, National Key Laboratory of Immune Response and Immunotherapy, Shanghai Institute of Immunity and Infection, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Dong DuanThe Center for Microbes, Development and Health, National Key Laboratory of Immune Response and Immunotherapy, Shanghai Institute of Immunity and Infection, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Yunyi LiShanghai Municipal Center for Disease Control and Prevention, Shanghai, China.
Xiaoxian CuiShanghai Municipal Center for Disease Control and Prevention, Shanghai, China.
Jiabin MouShanghai Municipal Center for Disease Control and Prevention, Shanghai, China.
Yuying YangShanghai Municipal Center for Disease Control and Prevention, Shanghai, China.
Xun WangShanghai Blood Center, Shanghai, China.
Min ChenShanghai Municipal Center for Disease Control and Prevention, Shanghai, China.
Yaming JiuThe Center for Microbes, Development and Health, National Key Laboratory of Immune Response and Immunotherapy, Shanghai Institute of Immunity and Infection, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Jincun ZhaoThe First Affiliated Hospital of Guangzhou Medical University, State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, Guangzhou, China.
Guangxun MengThe Center for Microbes, Development and Health, National Key Laboratory of Immune Response and Immunotherapy, Shanghai Institute of Immunity and Infection, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.ORCID https://orcid.org/0000-0003-4634-4661

Funding

China Postdoctoral Science Foundation 2024M763413Chinese Academy of Sciences Strategic Priority Research Program XDB0940102Guangdong Basic and Applied Basic Research Foundation 2023A1515010152National Key Research and Development Program of China 2022YFC2303200National Key Research and Development Program of China 2022YFC2303502National Natural Science Foundation of China 82402593National Natural Science Foundation of China 82825001National Natural Science Foundation of China 92054104National Natural Science Foundation of China 92269202Shanghai Municipal Science and Technology Major Project 2019SHZDZX02State Key Laboratory of Respiratory Disease J24411029Three-Year Initiative Plan for Strengthening Public Health System Construction in Shanghai (2023-2025) Key Discipline Project GWVI-11.1-09Young Scientist Fund of the Guangzhou National Laboratory QNPG23-03
6 · The paper itself

Abstract

Innate immune responses triggered by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection play pivotal roles in the pathogenesis of COVID-19, while host factors including proinflammatory cytokines are critical for viral containment. By utilizing quantitative and qualitative models, we discovered that soluble factors secreted by human monocytes potently inhibit SARS-CoV-2-induced cell-cell fusion in viral-infected cells. Through cytokine screening, we identified that interleukin-1β (IL-1β), a key mediator of inflammation, inhibits syncytia formation mediated by various SARS-CoV-2 strains. Mechanistically, IL-1β activates RhoA/ROCK signaling through a non-canonical IL-1 receptor-dependent pathway, which drives the enrichment of actin bundles at the cell-cell junctions, thus prevents syncytia formation. Notably, in vivo infection experiments in mice confirmed that IL-1β significantly restricted SARS-CoV-2 spread in the lung epithelium. Together, by revealing the function and underlying mechanism of IL-1β on SARS-CoV-2-induced cell-cell fusion, our study highlights an unprecedented antiviral function for cytokines during viral infection.

Indexed as

ActinsCOVID-19Interleukin-1betaMembrane FusionSARS-CoV-2Virus InternalizationAnimalsCell FusionGiant CellsHumansMiceMonocytesSignal TransductionActinsInterleukin-1betaactin bundlecell-cell fusionhumanimmunologyinfectious diseaseinflammationinnate immune cellinterlukin-1microbiologymouseSARS-CoV-2

Identifiers

PMID39937682
PMCPMC11820142

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.