ArticleCell reports2025
Viral insulin/IGF-like peptides inhibit IGF-1 receptor signaling to enhance viral replication.
Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Antibody-Based Biologics for CNS Disorders.Antibodies (Basel, Switzerland) · 2026Review
- Evolution of Insulin, Insulin-like Growth Factors, and Their Cognate Receptors in Vertebrates, Invertebrates, and Viruses.Molecular biology and evolution · 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
14 authors.
Funding
Abstract
The insulin/insulin growth factor (IGF) system plays a central role in regulating metabolism and growth. We identified viral insulin/IGF1-like peptides (VILPs) in Iridoviridae and investigated their role in host-virus interactions. Using grouper iridovirus (GIV) on grouper and zebrafish cells, we show that VILPs are early viral genes and are secreted during infection. VILPs activate insulin receptor (IR) and IGF-1 receptor (IGF1R) phosphorylation and stimulate the phosphatidylinositol 3-kinase (PI3K) pathway. GIV-VILP present in the supernatants of infected cells triggers dose- and time-dependent signaling through selective interaction with IGF1R. Functionally, IR inhibition suppresses GIV replication, whereas IGF1R inhibition enhances it, and IGF-1 stimulation reduces replication. During infection, GIV-VILP competes with IGF-1, attenuating IGF1R signaling and reducing proliferation. Transcriptome analysis confirms negative regulation of cell cycle pathways. Using a zebrafish infection model, we demonstrate VILP expression and IGF-1 signaling inhibition. Our findings reveal a viral mimicry mechanism that modulates host IGF-1 signaling to promote viral replication.
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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.