ArticleVirologica Sinica2023
RIPK3 promotes hantaviral replication by restricting JAK-STAT signaling without triggering necroptosis.
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 5 papers.
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Who cites it
5 citing papers in PubMed, 4 citations in OpenAlex.
- Integrated Downstream Analysis and Epidemiological Modelling of Hantavirus Infection: From Host Transcriptomics to Transmission Dynamics.Pathogens (Basel, Switzerland) · 2026Article
- ORF3 protein of porcine circovirus type 2 induced RIPK3 phosphorylation-driven autophagy to promote viral replication.Scientific reports · 2026Article
- Correlating hemorrhagic fever with renal syndrome incidence and research publications in China: insights from epidemiological and bibliometric analysis.One health outlook · 2025Article
- Aptamers as Potential Inhibitors of Ethylene Biosynthesis: Identification and In Silico Selection.International journal of molecular sciences · 2025Article
- Differential tropisms of old and new world hantaviruses influence virulence and developing host-directed antiviral candidates.PLoS pathogens · 2025Article
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Authors and funding
17 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hantaan virus (HTNV) is a rodent-borne virus that causes hemorrhagic fever with renal syndrome (HFRS), resulting in a high mortality rate of 15%. Interferons (IFNs) play a critical role in the anti-hantaviral immune response, and IFN pretreatment efficiently restricts HTNV infection by triggering the expression of a series of IFN-stimulated genes (ISGs) through the Janus kinase-signal transducer and activator of transcription 1 (JAK-STAT) pathway. However, the tremendous amount of IFNs produced during late infection could not restrain HTNV replication, and the mechanism remains unclear. Here, we demonstrated that receptor-interacting protein kinase 3 (RIPK3), a crucial molecule that mediates necroptosis, was activated by HTNV and contributed to hantavirus evasion of IFN responses by inhibiting STAT1 phosphorylation. RNA-seq analysis revealed the upregulation of multiple cell death-related genes after HTNV infection, with RIPK3 identified as a key modulator of viral replication. RIPK3 ablation significantly enhanced ISGs expression and restrained HTNV replication, without affecting the expression of pattern recognition receptors (PRRs) or the production of type I IFNs. Conversely, exogenously expressed RIPK3 compromised the host's antiviral response and facilitated HTNV replication. RIPK3
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