ArticleVirologica Sinica2023
STING strengthens host anti-hantaviral immunity through an interferon-independent pathway.
Article in Virologica Sinica, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- cGAS-STING pathway modulation: A new hope for neural regeneration.Neural regeneration research · 2026Article
- STING is a key driver of Japanese encephalitis virus induced inflammatory response.Communications biology · 2026Article
- PRRSV evades innate immune cGAS-STING antiviral function via its Nsp5 to deter STING translocation and activation.Virulence · 2025Article
- STING activates ZBP1-mediated PANoptosis to defend against HSV-1 retinal infection.Journal of neuroinflammation · 2025Article
- Differential tropisms of old and new world hantaviruses influence virulence and developing host-directed antiviral candidates.PLoS pathogens · 2025Article
- Research and progress of cGAS/STING/NLRP3 signaling pathway: a mini review.Frontiers in immunology · 2025Review
- Comprehensive analysis of genes associated with necroptosis and pyroptosis in intestinal ischemia-reperfusion injury.PloS one · 2025Article
- Suppression of Interferon Response and Antiviral Strategies of Bunyaviruses.Tropical medicine and infectious disease · 2024Review
- Stimulator of Interferon Gene Agonists Induce an Innate Antiviral Response against Influenza Viruses.Viruses · 2024Article
- Innate immune response against vector-borne bunyavirus infection and viral countermeasures.Frontiers in cellular and infection microbiology · 2024Review
Corrections and comments
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Authors and funding
19 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hantaan virus (HTNV), the prototype virus of hantavirus, could escape innate immunity by restraining type I interferon (IFN) responses. It is largely unknown whether there existed other efficient anti-hantaviral tactics in host cells. Here, we demonstrate that the stimulator of interferon genes (STING) strengthens the host IFN-independent anti-hantaviral immunity. HTNV infection activates RIG-I through IRE1-XBP 1-mediated ER stress, which further facilitates the subcellular translocation and activation of STING. During this process, STING triggers cellular autophagy by interacting with Rab7A, thus restricting viral replication. To note, the anti-hantaviral effects of STING are independent of canonical IFN signaling. Additionally, neither application of the pharmacological antagonist nor the agonist targeting STING could improve the outcomes of nude mice post HTNV challenge in vivo. However, the administration of plasmids exogenously expressing the mutant C-terminal tail (ΔCTT) STING, which would not trigger the type I IFN responses, protected the nude mice from lethal HTNV infection. In summary, our research revealed a novel antiviral pathway through the RIG-I-STING-autophagy pathway, which offered novel therapeutic strategies against hantavirus infection.
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