ArticleFrontiers in cellular and infection microbiology2022
Dengue virus downregulates TNFR1- and TLR3-stimulated NF-κB activation by targeting RIPK1.
Article in Frontiers in cellular and infection microbiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Magnolol Modulates the RIG-I/NF-κB Signaling Pathway to Alleviate JEV Infection-Induced ST Cell Damage.Animals : an open access journal from MDPI · 2026Article
- The Flavivirus NS3 Protein: Its Multifaceted Roles and Therapeutic Potential.Journal of medical virology · 2026Review
- Exploiting host kinases to combat dengue virus infection and disease.Antiviral research · 2025Review
- From defense to offense: Modulating toll-like receptors to combat arbovirus infections.Human vaccines & immunotherapeutics · 2024Review
- Transcriptome Analysis of Porcine Immune Cells Stimulated by Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) andInternational journal of molecular sciences · 2024Article
- Multiple receptor tyrosine kinases regulate dengue infection of hepatocytes.Frontiers in cellular and infection microbiology · 2024Article
- The natural compound Sanggenon C inhibits PRRSV infection by regulating the TRAF2/NF-κB signalling pathway.Veterinary research · 2023Article
- Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Dengue virus (DENV) infection is the most prevalent arthropod-borne virus disease and is endemic in more than 100 countries. Several DENV proteins have been shown to target crucial human host proteins to evade innate immune responses and establish a productive infection. Here we report that the DENV NS3 protein targets RIPK1 (Receptor Interacting Protein Kinase I), a central mediator of inflammation and cell death, and decreases intracellular RIPK1 levels during DENV infection. The interaction of NS3 with RIPK1 results in the inhibition of NF-κB activation in response to TNFR or TLR3 stimulation. Also, we observed that the effects of NS3 on RIPK1 were independent of NS3 protease activity. Our data demonstrate a novel mechanism by which DENV suppresses normal cellular functions to evade host innate immune responses.
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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.