ArticlePLoS pathogens2023
An aquatic virus exploits the IL6-STAT3-HSP90 signaling axis to promote viral entry.
Article in PLoS pathogens, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 33 citations in OpenAlex.
- Article
- Article
- The Role of Gut Microbiota in Fish Viral Infection: Mechanisms and Microbiota-Targeted Interventions.Aquaculture nutrition · 2026Review
- Helicobacter hepaticus promotes hepatic steatosis through CdtB-induced mitochondrial stress and lipid metabolism reprogramming.Nature communications · 2025Article
- Cold-blooded vertebrates evolved regulatory B cells to participate in inflammatory diseases.Cell communication and signaling : CCS · 2025Article
- Type II grass carp reovirus utilizes autophagosomes for viroplasm formation and subclinical persistent infection.Journal of virology · 2025Article
- The regulatory roles of STAT3 protein in the pathogenesis of viral infections.Frontiers in cellular and infection microbiology · 2025Review
- Expression of NEAT1 induced by influenza virus infection is regulated by activated STAT3 and contributes to STAT3-mediated antiviral immunity.Frontiers in immunology · 2025Article
- Parabacteroides distasonis regulates the infectivity and pathogenicity of SVCV at different water temperatures.Microbiome · 2024Article
- GCRV-II invades monocytes/macrophages and induces macrophage polarization and apoptosis in tissues to facilitate viral replication and dissemination.Journal of virology · 2024Article
- The impact of interleukin-6 (IL-6) and mesenchymal stem cell-derived IL-6 on neurological conditions.Frontiers in immunology · 2024Review
- Correction: An aquatic virus exploits the IL6-STAT3-HSP90 signaling axis to promote viral entry.PLoS pathogens · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Viral seasonality in the aquaculture industry is an important scientific issue for decades. While the molecular mechanisms underpinning the temperature-dependent pathogenesis of aquatic viral diseases remain largely unknown. Here we report that temperature-dependent activation of IL6-STAT3 signaling was exploited by grass carp reovirus (GCRV) to promote viral entry via increasing the expression of heat shock protein 90 (HSP90). Deploying GCRV infection as a model system, we discovered that GCRV induces the IL6-STAT3-HSP90 signaling activation to achieve temperature-dependent viral entry. Further biochemical and microscopic analyses revealed that the major capsid protein VP7 of GCRV interacted with HSP90 and relevant membrane-associated proteins to boost viral entry. Accordingly, exogenous expression of either IL6, HSP90, or VP7 in cells increased GCRV entry in a dose-dependent manner. Interestingly, other viruses (e.g., koi herpesvirus, Rhabdovirus carpio, Chinese giant salamander iridovirus) infecting ectothermic vertebrates have evolved a similar mechanism to promote their infection. This work delineates a molecular mechanism by which an aquatic viral pathogen exploits the host temperature-related immune response to promote its entry and replication, instructing us on new ways to develop targeted preventives and therapeutics for aquaculture viral diseases.
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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.