ArticlePLoS pathogens2010
Rabies virus infection induces type I interferon production in an IPS-1 dependent manner while dendritic cell activation relies on IFNAR signaling.
Article in PLoS pathogens, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 115 citations in OpenAlex.
- Targeting pattern recognition receptors for cancer therapy: Mechanisms and strategies.Acta pharmaceutica Sinica. B · 2025Review
- A comparative analysis of the dendritic cell response upon exposure to different rabies virus strains.PLoS neglected tropical diseases · 2025Article
- Established and Emerging Roles of DEAD/H-Box Helicases in Regulating Infection and Immunity.Immunological reviews · 2025Review
- Structural Heterogeneity of the Rabies Virus Virion.Viruses · 2024Article
- Host Factors Modulate Virus-Induced IFN Production via Pattern Recognition Receptors.Journal of inflammation research · 2024Review
- Transcriptome analysis of salivary glands of rabies-virus-infected mice.Frontiers in microbiology · 2024Article
- TRIM21 Promotes Rabies Virus Production by Degrading IRF7 through Ubiquitination.International journal of molecular sciences · 2023Article
- Rabies virus uniquely reprograms the transcriptome of human monocyte-derived macrophages.Frontiers in cellular and infection microbiology · 2023Article
- Human BST2 inhibits rabies virus release independently of cysteine-linked dimerization and asparagine-linked glycosylation.PloS one · 2023Article
- Substitution of S179P in the Lyssavirus Phosphoprotein Impairs Its Interferon Antagonistic Function.Journal of virology · 2022Article
- Regulation of antiviral innate immunity by chemical modification of viral RNA.Wiley interdisciplinary reviews. RNA · 2022Review
- Regulation of innate immune responses by rabies virus.Animal models and experimental medicine · 2022Review
- Friend or foe: RIG- I like receptors and diseases.Autoimmunity reviews · 2022Review
- RIG-I-like Receptor Regulation of Immune Cell Function and Therapeutic Implications.Journal of immunology (Baltimore, Md. : 1950) · 2022Review
- Hsp90 Activity Is Necessary for the Maturation of Rabies Virus Polymerase.International journal of molecular sciences · 2022Article
- Reduced IFN-ß inhibitory activity of Lagos bat virus phosphoproteins in human compared to Eidolon helvum bat cells.PloS one · 2022Article
- Innate Immune Signaling and Role of Glial Cells in Herpes Simplex Virus- and Rabies Virus-Induced Encephalitis.Viruses · 2021Review
- Toll-Like Receptor 4 Regulates Rabies Virus-Induced Humoral Immunity through Recruitment of Conventional Type 2 Dendritic Cells to Lymph Organs.Journal of virology · 2021Article
- Establishment of Human-Induced Pluripotent Stem Cell-Derived Neurons-A Promising In Vitro Model for a Molecular Study of Rabies Virus and Host Interaction.International journal of molecular sciences · 2021Article
- Review
5 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
As with many viruses, rabies virus (RABV) infection induces type I interferon (IFN) production within the infected host cells. However, RABV has evolved mechanisms by which to inhibit IFN production in order to sustain infection. Here we show that RABV infection of dendritic cells (DC) induces potent type I IFN production and DC activation. Although DCs are infected by RABV, the viral replication is highly suppressed in DCs, rendering the infection non-productive. We exploited this finding in bone marrow derived DCs (BMDC) in order to differentiate which pattern recognition receptor(s) (PRR) is responsible for inducing type I IFN following infection with RABV. Our results indicate that BMDC activation and type I IFN production following a RABV infection is independent of TLR signaling. However, IPS-1 is essential for both BMDC activation and IFN production. Interestingly, we see that the BMDC activation is primarily due to signaling through the IFNAR and only marginally induced by the initial infection. To further identify the receptor recognizing RABV infection, we next analyzed BMDC from Mda-5-/- and RIG-I-/- mice. In the absence of either receptor, there is a significant decrease in BMDC activation at 12h post infection. However, only RIG-I-/- cells exhibit a delay in type I IFN production. In order to determine the role that IPS-1 plays in vivo, we infected mice with pathogenic RABV. We see that IPS-1-/- mice are more susceptible to infection than IPS-1+/+ mice and have a significantly increased incident of limb paralysis.
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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.