ArticleNpj viruses2026
The soluble G protein of respiratory syncytial virus promotes viral dissemination via TLR2-mediated NLRP3 priming and pyroptosis.
Article in Npj viruses, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- Review
- Rational design 2.0: transitioning from static structural biology to computational prioritization and iterative vaccine optimization for RSV.Frontiers in immunology · 2026Review
- When defense backfires: inflammatory determinants of RSV-induced disease severity.Future virology · 2026Article
- Unraveling the dual immunomodulatory and immunogenic roles of the central conserved cysteine-rich region in respiratory syncytial virus G protein.Frontiers in microbiology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Respiratory syncytial virus (RSV) causes severe lower respiratory tract infections in infants, immunocompromised individuals, and older adults. Although vaccines and monoclonal antibodies have recently become available, understanding RSV pathogenesis remains essential for next-generation therapeutic strategies. RSV attachment glycoprotein G mediates virus binding through a CX3C-like chemokine motif, and its secreted soluble form (sG) possesses immunomodulatory properties. We showed that recombinant sG binds TLR2, inducing proinflammatory mediators. In vitro, sG pretreatment of airway epithelial cells enhanced viral replication upon infection, indicating functions beyond canonical receptor binding. We demonstrated that RSV sG can activate MyD88-NF-κB signalling in uninfected cells via TLR2, leading to NLRP3 upregulation and ROS accumulation. Subsequent RSV infection provides the second signal for caspase‑1 activation and pyroptosis, preconditioning neighbouring cells for inflammasome-dependent lysis and viral egress. Targeting the sG-TLR2 interface could reduce inflammatory damage and viral spread, providing a rationale for CX3C motif-directed interventions and NLRP3 inhibitors during infection.
Identifiers
What OpenQuestion holds
Registered trials
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.