ArticleCell insight2026
TNF inhibits SARS-CoV-2 induced cell-cell fusion through activating the SDC4-RhoA signaling to promote actin bundles formation.
Article in Cell insight, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.
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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.
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.
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Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
- Erratum issued
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SARS-CoV-2 infection-induced syncytia formation accelerates cell-to-cell transmission of the virus and enhances viral evasion by neutralizing antibodies. Host innate immune response plays a key role in controlling viral infection. Our present work identifies tumor necrosis factor (TNF) as a key cytokine quickly released from activated innate immune cells that suppresses SARS-CoV-2 spike-mediated cell-cell fusion. Mechanistically, TNF signals through the TNFR1-TRADD/TRAF2/RIPK1-MAPK-SDC4 axis. SDC4 further activates the RhoA/ROCK signaling pathway, which promotes cytoskeletal reorganization, leading to the formation of actin bundles at the interface between infected cell and adjacent cell. Such remodeling of actin effectively blocks further propagation of syncytia and viral spreading. These findings provide critical insights into the dynamic interplay between host antiviral factors and syncytia formation, deepening our understanding of the innate immune control of SARS-CoV-2 infection.
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