ArticleJournal of virology2009
Host responses to wild-type and attenuated herpes simplex virus infection in the absence of Stat1.
Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
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Who cites it
31 citing papers in PubMed, 41 citations in OpenAlex.
- Intranasal HSV‑1 infection drives region‑specific interferon‑dominant microglial remodeling.PLoS pathogens · 2026Article
- STAT1 and herpesviruses: Making lemonade from lemons.Virology · 2025Review
- The immunobiology of corneal HSV-1 infection and herpetic stromal keratitis.Clinical microbiology reviews · 2024Review
- Article
- Essential role of M1 macrophages in blocking cytokine storm and pathology associated with murine HSV-1 infection.PLoS pathogens · 2021Article
- Viral infections in humans and mice with genetic deficiencies of the type I IFN response pathway.European journal of immunology · 2021Review
- "Non-Essential" Proteins of HSV-1 with Essential Roles In Vivo: A Comprehensive Review.Viruses · 2020Review
- Insights into the pathogenesis of herpes simplex encephalitis from mouse models.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Review
- IL-6 Contributes to Corneal Nerve Degeneration after Herpes Simplex Virus Type I Infection.The American journal of pathology · 2016Article
- Functional prediction of differentially expressed lncRNAs in HSV-1 infected human foreskin fibroblasts.Virology journal · 2016Article
- The Herpes Simplex Virus Virion Host Shutoff Protein Enhances Translation of Viral True Late mRNAs Independently of Suppressing Protein Kinase R and Stress Granule Formation.Journal of virology · 2016Article
- Cellular responses to HSV-1 infection are linked to specific types of alterations in the host transcriptome.Scientific reports · 2016Article
- 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
- Cellular Protein WDR11 Interacts with Specific Herpes Simplex Virus Proteins at the trans-Golgi Network To Promote Virus Replication.Journal of virology · 2015Article
- Degeneration and regeneration of corneal nerves in response to HSV-1 infection.Investigative ophthalmology & visual science · 2015Article
- The differential interferon responses of two strains of Stat1-deficient mice do not alter susceptibility to HSV-1 and VSV in vivo.Virology · 2014Article
- Herpes simplex virus 1 counteracts tetherin restriction via its virion host shutoff activity.Journal of virology · 2013Article
- Genome-wide mouse mutagenesis reveals CD45-mediated T cell function as critical in protective immunity to HSV-1.PLoS pathogens · 2013Article
- Synergistic control of herpes simplex virus pathogenesis by IRF-3, and IRF-7 revealed through non-invasive bioluminescence imaging.Virology · 2013Article
- Modeling host genetic regulation of influenza pathogenesis in the collaborative cross.PLoS pathogens · 2013Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Humans and mice lacking the interferon signaling molecule Stat1 are sensitive to a variety of pathogens due to their presumed inability to mount a strong innate immune response. The herpes simplex virus type 1 (HSV-1) virion host shutoff (vhs) protein is a multifunctional immunomodulator that counteracts the innate immune response and viruses lacking vhs are attenuated and effective live vaccines in animal models. To investigate the interplay of viruses with an immunocompromised host, we performed functional genomics analyses on control and Stat1(-/-) mouse corneas infected with wild-type or vhs-null viruses. In control mice, correlative with viral growth, both viruses induced a transient increase in immunomodulators, followed by viral clearance. In contrast, infection of the Stat1(-/-) mice induced a heightened and prolonged induction of inflammatory modulators for both viruses, manifesting as a significant immune cell infiltrate and ocular disease. Moreover, while wild-type virus infection of Stat1(-/-) was always lethal, vhs-null infection was rarely lethal. There was a significant increase in Stat3- and interleukin-6 (IL-6)-dependent transcription in Stat1(-/-) mice, implicating the Stat3 and IL-6 pathways in the observed ocular pathology. Further, infected Stat1(-/-) mice showed phosphorylated Stat3 in the corneal epithelium. Our data show a role for vhs in evading innate host responses and a role for Stat1 in limiting virus infection and for facilitating an appropriate nonpathological inflammatory response.
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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.