ArticlePLoS pathogens2025
ZNFX1 functions as a compensatory dsRNA recognition receptor to exert antiviral effect in orange-spotted grouper.
Article in PLoS pathogens, 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.
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Who cites it
2 citing papers in PubMed.
- Zebrafish larvae reveal early neuropathology and host responses to nervous necrosis virus.iScience · 2026Article
- Pollution-driven viral susceptibility: mixed contaminants as hidden determinants of aquaculture disease.Advanced biotechnology · 2025Article
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Authors and funding
8 authors.
Funding
Abstract
Zinc finger NFX1-type containing 1 (ZNFX1) has been established as a critical mediator of the antiviral response in mammals, functioning through dsRNA recognition and priority activation of the retinoic acid-inducible gene I (RIG-I)-like receptor (RLR) signaling pathway. However, the role of its fish ortholog, particularly in relation to aquatic virus interactions, remains elusive. The absence of the RIG-I homolog, a key pattern recognition receptor, in multiple Actinopterygii may compromise their innate antiviral immune responses. Here, ZNFX1 in Epinephelus coioides (EcZNFX1) is identified as an evolutionarily primitive, interferon (IFN)-stimulated dsRNA sensor that compensates for the absence of RIG-I in Actinopterygii. EcZNFX1 is rapidly upregulated by orange-spotted grouper nervous necrosis virus (OGNNV) infection and restricts viral replication in grouper brain-derived (GB) and spleen-derived (GS) cells after binding to viral dsRNA intermediates via its conserved P-loop NTPase domain. Notably, EcZNFX1 exerts a dual immunoregulatory role in modulating virus-induced inflammatory responses in diverse cellular contexts. In GB cells that are highly susceptible to OGNNV and have attenuated regenerative capacity, EcZNFX1 suppresses IFN-I/ISGs production and pyroptosis mediated by viral infection, thereby limiting neurotoxicity by precise tuning of the antiviral response. Conversely, in GS cells with stronger resistance to OGNNV, EcZNFX1 directly interacts with TBK1 to promote its phosphorylation and subsequent nuclear translocation of IRF3, activating a robust IFN-I signaling. Overall, this study elucidates that ZNFX1 is a compensatory receptor for dsRNA sensing in RIG-I-deficient teleost, which exerts context-dependent antiviral effects in cell-type-specific microenvironments, providing mechanistic insights for aquatic virus countermeasures.
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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 Socratic graph.