ArticleJournal of virology2010
Interferon regulatory factor 3-dependent pathways are critical for control of herpes simplex virus type 1 central nervous system infection.
Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
39 citing papers in PubMed, 47 citations in OpenAlex.
- RIPK3 acts as a molecular switch between neuroprotection and neuropathology during herpes simplex encephalitis.Nature communications · 2026Article
- Interferon-Stimulated Gene-Mediated Defense Against Prion Infection: Noncanonical Function of Oas1a.Viruses · 2026Review
- IRF3 in viral infections: more than just triggering the interferon response.Genes and immunity · 2025Review
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- IRF3 inhibits nuclear translocation of NF-κB to prevent viral inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Microglia Activate Early Antiviral Responses upon Herpes Simplex Virus 1 Entry into the Brain to Counteract Development of Encephalitis-Like Disease in Mice.Journal of virology · 2022Article
- Interactive effect of TLR SNPs and exposure to sexually transmitted infections on prostate cancer risk in Jamaican men.The Prostate · 2020Article
- Pathological processes activated by herpes simplex virus-1 (HSV-1) infection in the cornea.Cellular and molecular life sciences : CMLS · 2019Review
- Interferon regulatory factors 3 and 7 have distinct roles in the pathogenesis of alphavirus encephalomyelitis.The Journal of general virology · 2019Article
- Both IRF3 and especially IRF7 play a key role to orchestrate an effective cerebral inflammatory response in a mouse model of herpes simplex virus encephalitis.Journal of neurovirology · 2018Article
- Revisiting the role of IRF3 in inflammation and immunity by conditional and specifically targeted gene ablation in mice.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- IRF and STAT Transcription Factors - From Basic Biology to Roles in Infection, Protective Immunity, and Primary Immunodeficiencies.Frontiers in immunology · 2018Review
- Role of Herpes Simplex Virus 1 γ34.5 in the Regulation of IRF3 Signaling.Journal of virology · 2017Article
- Differentiated Human SH-SY5Y Cells Provide a Reductionist Model of Herpes Simplex Virus 1 Neurotropism.Journal of virology · 2017Article
- Immune- and Nonimmune-Compartment-Specific Interferon Responses Are Critical Determinants of Herpes Simplex Virus-Induced Generalized Infections and Acute Liver Failure.Journal of virology · 2016Article
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- Article
- A NK complex-linked locus restricts the spread of herpes simplex virus type 1 in the brains of C57BL/6 mice.Immunology and cell biology · 2015Article
- Role of the DNA Sensor STING in Protection from Lethal Infection following Corneal and Intracerebral Challenge with Herpes Simplex Virus 1.Journal of virology · 2015Article
- Innate immune interactions within the central nervous system modulate pathogenesis of viral infections.Current opinion in immunology · 2015Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The initiation of the immune response at the cellular level relies on specific recognition molecules to rapidly signal viral infection via interferon (IFN) regulatory factor 3 (IRF-3)-dependent pathways. The absence of IRF-3 would be expected to render such pathways inoperative and thereby significantly affect viral infection. Unexpectedly, a previous study found no significant change in herpes simplex virus (HSV) pathogenesis in IRF-3(-/-) mice following intravenous HSV type 1 (HSV-1) challenge (K. Honda, H. Yanai, H. Negishi, M. Asagiri, M. Sato, T. Mizutani, N. Shimada, Y. Ohba, A. Takaoka, N. Yoshida, and T. Taniguchi, Nature 434:772-777, 2005). In contrast, the present study demonstrated that IRF-3(-/-) mice are significantly more susceptible to HSV infection via the corneal and intracranial routes. Following corneal infection with 2 x 10(6) PFU of HSV-1 strain McKrae, 50% of wild-type mice survived, compared to 10% of IRF-3-deficient mice. Significantly increased viral replication and inflammatory cytokine production were observed in brain tissues of IRF-3(-/-) mice compared to control mice, with a concomitant deficit in production of both IFN-beta and IFN-alpha. These data demonstrate a critical role for IRF-3 in control of central nervous system infection following HSV-1 challenge. Furthermore, this work underscores the necessity to evaluate multiple routes of infection and animal models in order to fully determine the role of host resistance factors in pathogenesis.
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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.